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Article: Loss of Serum Glucocorticoid-Inducible Kinase 1 SGK1 Worsens Malabsorption and Diarrhea in Microvillus Inclusion Disease (MVID).

Ahsan, Md Kaimul / Dos Reis, Diego Carlos / Barbieri, Andrea / Sumigray, Kaelyn D / Nottoli, Timothy / Salas, Pedro J / Ameen, Nadia A

Journal of clinical medicine

2022 Volume 11, Issue 14

Abstract: Microvillus inclusion disease (MVID), a lethal congenital diarrheal disease, results from loss of function mutations in the apical actin motor myosin VB (MYO5B). How loss of MYO5B leads to both malabsorption and fluid secretion is not well understood. ... ...

Abstract	Microvillus inclusion disease (MVID), a lethal congenital diarrheal disease, results from loss of function mutations in the apical actin motor myosin VB (MYO5B). How loss of MYO5B leads to both malabsorption and fluid secretion is not well understood. Serum glucocorticoid-inducible kinase 1 (SGK1) regulates intestinal carbohydrate and ion transporters including cystic fibrosis transmembrane conductance regulator (CFTR). We hypothesized that loss of SGK1 could reduce CFTR fluid secretion and MVID diarrhea. Using CRISPR-Cas9 approaches, we generated R26
Language	English
Publishing date	2022-07-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662592-1
ISSN	2077-0383
ISSN	2077-0383
DOI	10.3390/jcm11144179
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Article: Activation of adenosine receptor A2A increases HSC proliferation and inhibits death and senescence by down-regulation of p53 and Rb.

Ahsan, Md Kaimul / Mehal, Wajahat Z

Frontiers in pharmacology

2014 Volume 5, Page(s) 69

Abstract: Background and aims: During fibrosis hepatic stellate cells (HSC) undergo activation, proliferation, and senescence but the regulation of these important processes is poorly understood. The adenosine A2A receptor (A2A) is known to be present on HSC, and ...

Abstract	Background and aims: During fibrosis hepatic stellate cells (HSC) undergo activation, proliferation, and senescence but the regulation of these important processes is poorly understood. The adenosine A2A receptor (A2A) is known to be present on HSC, and its activation results in liver fibrosis. In this study, we tested if A2A has a role in the regulation of HSC proliferation, apoptosis, senescence, and the relevant molecular mechanism. Methods: The ability of adenosine to regulate p53 and Rb protein levels, proliferation, apoptosis and senescence was tested in the human HSC cell line LX-2 and rat primary HSC. Results: Adenosine receptor activation down-regulates p53 and Rb protein levels, increases BrdU incorporation and increases cell survival in LX-2 cells and in primary rat HSC. These effects of NECA were reproduced by an adenosine A2A receptor specific agonist (CGS21680) and blocked by a specific antagonist (ZM241385). By day twenty-one of culture primary rat HSC entered senescence and expressed β-gal which was significantly inhibited by NECA. Furthermore, NECA induced down regulation of p53 and Rb and Rac1, and decreased phosphorylation of p44-42 MAP Kinase in LX-2 cells and primary rat HSC. These effects were reproduced by the cAMP analog 8-Bromo-cAMP, and the adenylyl cyclase activator forskolin, and were blocked by PKA inhibitors. Conclusions: These results demonstrate that A2A receptor regulates a number of HSC fate decisions and induces greater HSC proliferation, reduces apoptosis and senescence by decreasing p53 and Rb through cAMP-PKA/Rac1/p38 MAPK pathway. This provides a mechanism for adenosine induced HSC regulation and liver fibrosis.
Language	English
Publishing date	2014-04-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2014.00069
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Article ; Online: Glucocorticoids and serum- and glucocorticoid-inducible kinase 1 are potent regulators of CFTR in the native intestine: implications for stress-induced diarrhea.

Ahsan, Md Kaimul / Figueroa-Hall, Leandra / Baratta, Vanessa / Garcia-Milian, Rolando / Lam, TuKiet T / Hoque, Kazi / Salas, Pedro J / Ameen, Nadia A

American journal of physiology. Gastrointestinal and liver physiology

2020 Volume 319, Issue 2, Page(s) G121–G132

Abstract: Nongenomic glucocorticoid (GC) and serum- and glucocorticoid-inducible kinase 1 (SGK1) signaling regulate ion transport, but CFTR has not been investigated in the intestine. We examined GC, SGK1, and phosphatidylinositol 3-kinase (PI3K) kinase signaling ... ...

Abstract	Nongenomic glucocorticoid (GC) and serum- and glucocorticoid-inducible kinase 1 (SGK1) signaling regulate ion transport, but CFTR has not been investigated in the intestine. We examined GC, SGK1, and phosphatidylinositol 3-kinase (PI3K) kinase signaling of CFTR ion transport in native intestine and the role of GCs on mRNA, protein, surface expression, and cyclic guanosine monophosphate (cGMP)-elicited diarrhea. Rats were treated with dexamethasone (DEXA; 2 mg/kg ip) or DMSO for 1, 4, and 24 h. Cyclic adenosine monophosphate (cAMP)-activated ion transport was examined in the presence or absence of SGK1 and PI3K inhibitors. Phosphorylation of SGK1, phosphoinositide-dependent kinase 1, and Akt kinases was confirmed by immunoblots using phosphor-specific antibodies. Tissue lysates were analyzed by mass spectrometry. CFTR and SGK1 mRNA were measured by quantitative PCR. Changes in total and surface CFTR protein were determined. The role of GC in cGMP-activated CFTR ion transport was examined. GC synergistically increased CFTR ion transport by SGK1 and PI3K signaling and increased CFTR protein without altering SGK1 or CFTR mRNA. GC induced highest levels of CFTR protein at 4 h that were associated with marked increase in surface CFTR, phosphorylation of the ubiquitin ligase neural precursor cell expressed developmentally downregulated 4-like (Nedd4-2), and 14-3-3ε, supporting their roles in surface retention and stability. Coimmunoprecipitation of CFTR, Nedd4-2, and 14-3-3ε indicated that assembly of this complex is a likely effector of the SGK and Akt pathways. Mass spectrometry identified phosphorylated peptides in relevant proteins. GC-SGK1 potently regulates CFTR in the intestine and is implicated in diarrheal disease.
MeSH term(s)	14-3-3 Proteins/genetics ; 14-3-3 Proteins/metabolism ; Animals ; Bacterial Toxins/toxicity ; Cystic Fibrosis Transmembrane Conductance Regulator/genetics ; Cystic Fibrosis Transmembrane Conductance Regulator/metabolism ; Dexamethasone/toxicity ; Diarrhea/chemically induced ; Diarrhea/etiology ; Dimethyl Sulfoxide/toxicity ; Enterotoxins/toxicity ; Escherichia coli Proteins/toxicity ; Gene Expression Regulation/drug effects ; Immediate-Early Proteins/genetics ; Immediate-Early Proteins/metabolism ; Male ; Nedd4 Ubiquitin Protein Ligases/genetics ; Nedd4 Ubiquitin Protein Ligases/metabolism ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Protein Serine-Threonine Kinases/genetics ; Protein Serine-Threonine Kinases/metabolism ; Protein Transport ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Pyruvate Dehydrogenase Acetyl-Transferring Kinase/genetics ; Pyruvate Dehydrogenase Acetyl-Transferring Kinase/metabolism ; Rats ; Rats, Sprague-Dawley ; Sodium-Hydrogen Exchanger 3/genetics ; Sodium-Hydrogen Exchanger 3/metabolism
Chemical Substances	14-3-3 Proteins ; Bacterial Toxins ; CFTR protein, rat ; Enterotoxins ; Escherichia coli Proteins ; Immediate-Early Proteins ; Pdk1 protein, rat ; Pyruvate Dehydrogenase Acetyl-Transferring Kinase ; Slc9a3 protein, rat ; Sodium-Hydrogen Exchanger 3 ; heat stable toxin (E coli) ; Cystic Fibrosis Transmembrane Conductance Regulator (126880-72-6) ; Dexamethasone (7S5I7G3JQL) ; NEDD4L protein, rat (EC 2.3.2.26) ; Nedd4 Ubiquitin Protein Ligases (EC 2.3.2.26) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; serum-glucocorticoid regulated kinase (EC 2.7.11.1) ; Dimethyl Sulfoxide (YOW8V9698H)
Language	English
Publishing date	2020-06-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603840-2
ISSN	1522-1547 ; 0193-1857
ISSN (online)	1522-1547
ISSN	0193-1857
DOI	10.1152/ajpgi.00076.2020
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Article ; Online: Linaclotide activates guanylate cyclase-C/cGMP/protein kinase-II-dependent trafficking of CFTR in the intestine.

Ahsan, Md Kaimul / Tchernychev, Boris / Kessler, Marco M / Solinga, Robert M / Arthur, David / Linde, Cristina I / Silos-Santiago, Inmaculada / Hannig, Gerhard / Ameen, Nadia A

Physiological reports

2017 Volume 5, Issue 11

Abstract: The transmembrane receptor guanylyl cyclase-C (GC-C), expressed on enterocytes along the intestine, is the molecular target of the GC-C agonist peptide linaclotide, an FDA-approved drug for treatment of adult patients with Irritable Bowel Syndrome with ... ...

Abstract	The transmembrane receptor guanylyl cyclase-C (GC-C), expressed on enterocytes along the intestine, is the molecular target of the GC-C agonist peptide linaclotide, an FDA-approved drug for treatment of adult patients with Irritable Bowel Syndrome with Constipation and Chronic Idiopathic Constipation. Polarized human colonic intestinal cells (T84, CaCo-2BBe) rat and human intestinal tissues were employed to examine cellular signaling and cystic fibrosis transmembrane conductance regulator (CFTR)-trafficking pathways activated by linaclotide using confocal microscopy, in vivo surface biotinylation, and protein kinase-II (PKG-II) activity assays. Expression and activity of GC-C/cGMP pathway components were determined by PCR, western blot, and cGMP assays. Fluid secretion as a marker of CFTR cell surface translocation was determined using in vivo rat intestinal loops. Linaclotide treatment (30 min) induced robust fluid secretion and translocation of CFTR from subapical compartments to the cell surface in rat intestinal loops. Similarly, linaclotide treatment (30 min) of T84 and CaCo-2BBe cells increased cell surface CFTR levels. Linaclotide-induced activation of the GC-C/cGMP/PKGII signaling pathway resulted in elevated intracellular cGMP and pVASP
MeSH term(s)	Animals ; Cell Line ; Cell Line, Tumor ; Cell Membrane/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Cyclic GMP/metabolism ; Cyclic GMP-Dependent Protein Kinase Type II/metabolism ; Cystic Fibrosis Transmembrane Conductance Regulator/metabolism ; Guanylyl Cyclase C Agonists/pharmacology ; Humans ; Intestinal Mucosa/drug effects ; Intestinal Mucosa/metabolism ; Male ; Peptides/pharmacology ; Protein Transport ; Rats ; Rats, Sprague-Dawley ; Receptors, Guanylate Cyclase-Coupled/metabolism ; Signal Transduction
Chemical Substances	Guanylyl Cyclase C Agonists ; Peptides ; Cystic Fibrosis Transmembrane Conductance Regulator (126880-72-6) ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11) ; Cyclic GMP-Dependent Protein Kinase Type II (EC 2.7.11.12) ; Receptors, Guanylate Cyclase-Coupled (EC 4.6.1.2) ; Cyclic GMP (H2D2X058MU) ; linaclotide (N0TXR0XR5X)
Language	English
Publishing date	2017-06-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	2724325-4
ISSN	2051-817X ; 2051-817X
ISSN (online)	2051-817X
ISSN	2051-817X
DOI	10.14814/phy2.13299
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Article ; Online: Modulation of microRNA 20b with resveratrol and longevinex is linked with their potent anti-angiogenic action in the ischaemic myocardium and synergestic effects of resveratrol and γ-tocotrienol.

Mukhopadhyay, Partha / Das, Somak / Ahsan, Md Kaimul / Otani, Hajime / Das, Dipak K

Journal of cellular and molecular medicine

2011 Volume 16, Issue 10, Page(s) 2504–2517

Abstract: Resveratrol, a constituent of red wine, and γ-tocotrienol, a constituent of palm oil are important for cardioprotection. Although microRNAs are known regulators for genes involved in cardiac remodelling, the regulatory pathway involving microRNA has not ... ...

Abstract	Resveratrol, a constituent of red wine, and γ-tocotrienol, a constituent of palm oil are important for cardioprotection. Although microRNAs are known regulators for genes involved in cardiac remodelling, the regulatory pathway involving microRNA has not been studied so far. We explored the cardioprotection by resveratrol, longevinex and γ-tocotrienol in ischaemia/reperfusion(I/R) model of rat and determined miRNA profile from isolated RNA. Systemic analyses of miRNA array and theirs targets were determined using a number of computational approaches. Resveratrol and γ-tocotrienol, either alone or in combination, modulated the expression pattern of miRNAs close to the control level based on PCA analyses. Differential expression was observed in over 75 miRNAs, some of them, such as miR-21 and miR-20b (anti-angiogenic) were previously implicated in cardiac remodelling. The target genes for the highest differentially expressed miRNA include genes of various molecular functions such as TGFβ1-Smad3 signalling pathway, inflammation and their transcription factors, which may play key role in reducing I/R injury. Administration of antagomiR-20 attenuated I/R induced vascular endothelial growth factor and HIF1α level. All the interventions treated for 3 weeks lead to significant cardioprotection against ischaemia/reperfusion injury. A unique signature of miRNA profile is observed in control heart pretreated with resveratrol or γ-tocotrienol. We have determined specific group of miRNA in heart that have altered during IR injuries. Most of those altered microRNA expressions modulated close to their basal level in resveratrol or longevinex treated I/R rat. Interestingly, resveratrol and γ-tocotrienol resulted in synergestic action.
MeSH term(s)	Angiogenesis Inhibitors/pharmacology ; Animals ; Apoptosis/drug effects ; Chromans/pharmacology ; Down-Regulation ; Drug Synergism ; Gene Expression Profiling/methods ; Heart/drug effects ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Male ; MicroRNAs/antagonists & inhibitors ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Microscopy, Confocal ; Multivariate Analysis ; Myocardial Ischemia/drug therapy ; Myocardial Ischemia/pathology ; Myocardium/pathology ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species/metabolism ; Resveratrol ; Signal Transduction ; Stilbenes/pharmacology ; Vascular Endothelial Growth Factor A/genetics ; Vascular Endothelial Growth Factor A/metabolism ; Vitamin E/analogs & derivatives ; Vitamin E/pharmacology
Chemical Substances	Angiogenesis Inhibitors ; Chromans ; Hif1a protein, rat ; Hypoxia-Inducible Factor 1, alpha Subunit ; MIRN20 microRNA, rat ; MicroRNAs ; Reactive Oxygen Species ; Stilbenes ; Vascular Endothelial Growth Factor A ; vascular endothelial growth factor A, rat ; Vitamin E (1406-18-4) ; plastochromanol 8 (4382-43-8) ; Resveratrol (Q369O8926L)
Language	English
Publishing date	2011-11-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	2074559-X
ISSN	1582-4934 ; 1582-4934 ; 1582-1838
ISSN (online)	1582-4934
ISSN	1582-4934 ; 1582-1838
DOI	10.1111/j.1582-4934.2011.01480.x
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Article ; Online: Identification of intestinal ion transport defects in microvillus inclusion disease.

Kravtsov, Dmitri V / Ahsan, Md Kaimul / Kumari, Vandana / van Ijzendoorn, Sven C D / Reyes-Mugica, Miguel / Kumar, Anoop / Gujral, Tarunmeet / Dudeja, Pradeep K / Ameen, Nadia A

American journal of physiology. Gastrointestinal and liver physiology

2016 Volume 311, Issue 1, Page(s) G142–55

Abstract: Loss of function mutations in the actin motor myosin Vb (Myo5b) lead to microvillus inclusion disease (MVID) and death in newborns and children. MVID results in secretory diarrhea, brush border (BB) defects, villus atrophy, and microvillus inclusions ( ... ...

Abstract	Loss of function mutations in the actin motor myosin Vb (Myo5b) lead to microvillus inclusion disease (MVID) and death in newborns and children. MVID results in secretory diarrhea, brush border (BB) defects, villus atrophy, and microvillus inclusions (MVIs) in enterocytes. How loss of Myo5b results in increased stool loss of chloride (Cl(-)) and sodium (Na(+)) is unknown. The present study used Myo5b loss-of-function human MVID intestine, polarized intestinal cell models of secretory crypt (T84) and villus resembling (CaCo2BBe, C2BBe) enterocytes lacking Myo5b in conjunction with immunofluorescence confocal stimulated emission depletion (gSTED) imaging, immunohistochemical staining, transmission electron microscopy, shRNA silencing, immunoblots, and electrophysiological approaches to examine the distribution, expression, and function of the major BB ion transporters NHE3 (Na(+)), CFTR (Cl(-)), and SLC26A3 (DRA) (Cl(-)/HCO3 (-)) that control intestinal fluid transport. We hypothesized that enterocyte maturation defects lead villus atrophy with immature secretory cryptlike enterocytes in the MVID epithelium. We investigated the role of Myo5b in enterocyte maturation. NHE3 and DRA localization and function were markedly reduced on the BB membrane of human MVID enterocytes and Myo5bKD C2BBe cells, while CFTR localization was preserved. Forskolin-stimulated CFTR ion transport in Myo5bKD T84 cells resembled that of control. Loss of Myo5b led to YAP1 nuclear retention, retarded enterocyte maturation, and a cryptlike phenotype. We conclude that preservation of functional CFTR in immature enterocytes, reduced functional expression of NHE3, and DRA contribute to Cl(-) and Na(+) stool loss in MVID diarrhea.
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Caco-2 Cells ; Chloride-Bicarbonate Antiporters/metabolism ; Cystic Fibrosis Transmembrane Conductance Regulator/metabolism ; Enterocytes/metabolism ; Enterocytes/ultrastructure ; Gene Expression Regulation ; Humans ; Ion Transport ; Jejunum/metabolism ; Jejunum/pathology ; Jejunum/ultrastructure ; Malabsorption Syndromes/genetics ; Malabsorption Syndromes/metabolism ; Malabsorption Syndromes/pathology ; Membrane Transport Proteins/genetics ; Membrane Transport Proteins/metabolism ; Microvilli/genetics ; Microvilli/metabolism ; Microvilli/pathology ; Microvilli/ultrastructure ; Mucolipidoses/genetics ; Mucolipidoses/metabolism ; Mucolipidoses/pathology ; Myosin Heavy Chains/genetics ; Myosin Heavy Chains/metabolism ; Myosin Type V/genetics ; Myosin Type V/metabolism ; Phenotype ; Phosphoproteins/metabolism ; RNA Interference ; Signal Transduction ; Sodium-Hydrogen Exchanger 3 ; Sodium-Hydrogen Exchangers/metabolism ; Sulfate Transporters ; Transcription Factors ; Transfection
Chemical Substances	Adaptor Proteins, Signal Transducing ; CFTR protein, human ; Chloride-Bicarbonate Antiporters ; MYO5B protein, human ; Membrane Transport Proteins ; Phosphoproteins ; SLC26A3 protein, human ; SLC9A3 protein, human ; Sodium-Hydrogen Exchanger 3 ; Sodium-Hydrogen Exchangers ; Sulfate Transporters ; Transcription Factors ; YAP1 protein, human ; Cystic Fibrosis Transmembrane Conductance Regulator (126880-72-6) ; Myosin Type V (EC 3.6.1.-) ; Myosin Heavy Chains (EC 3.6.4.1)
Language	English
Publishing date	2016-05-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	603840-2
ISSN	1522-1547 ; 0193-1857
ISSN (online)	1522-1547
ISSN	0193-1857
DOI	10.1152/ajpgi.00041.2016
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Article ; Online: Redox regulation of cell survival by the thioredoxin superfamily: an implication of redox gene therapy in the heart.

Ahsan, Md Kaimul / Lekli, Istvan / Ray, Diptarka / Yodoi, Junji / Das, Dipak K

Antioxidants & redox signaling

2009 Volume 11, Issue 11, Page(s) 2741–2758

Abstract: Reactive oxygen species (ROS) are the key mediators of pathogenesis in cardiovascular diseases. Members of the thioredoxin superfamily take an active part in scavenging reactive oxygen species, thus playing an essential role in maintaining the ... ...

Abstract	Reactive oxygen species (ROS) are the key mediators of pathogenesis in cardiovascular diseases. Members of the thioredoxin superfamily take an active part in scavenging reactive oxygen species, thus playing an essential role in maintaining the intracellular redox status. The alteration in the expression levels of thioredoxin family members and related molecules constitute effective biomarkers in various diseases, including cardiovascular complications that involve oxidative stress. Thioredoxin, glutaredoxin, peroxiredoxin, and glutathione peroxidase, along with their isoforms, are involved in interaction with the members of metabolic and signaling pathways, thus making them attractive targets for clinical intervention. Studies with cells and transgenic animals have supported this notion and raised the hope for possible gene therapy as modern genetic medicine. Of all the molecules, thioredoxins, glutaredoxins, and peroxiredoxins are emphasized, because a growing body of evidence reveals their essential and regulatory role in several steps of redox regulation. In this review, we discuss some pertinent observations regarding their distribution, structure, functions, and interactions with the several survival- and death-signaling pathways, especially in the myocardium.
MeSH term(s)	Animals ; Cell Survival/genetics ; Cell Survival/physiology ; Genetic Therapy ; Glutaredoxins/metabolism ; Glutaredoxins/physiology ; Humans ; Models, Biological ; Myocardium/metabolism ; Oxidation-Reduction ; Peroxiredoxins/metabolism ; Peroxiredoxins/physiology ; Signal Transduction/genetics ; Signal Transduction/physiology ; Thioredoxins/metabolism ; Thioredoxins/physiology
Chemical Substances	Glutaredoxins ; Thioredoxins (52500-60-4) ; Peroxiredoxins (EC 1.11.1.15)
Language	English
Publishing date	2009-07-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ARS.2009.2683
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Article ; Online: Thioredoxin and thioredoxin binding protein 2 in the liver.

Okuyama, Hiroaki / Son, Aoi / Ahsan, Md Kaimul / Masutani, Hiroshi / Nakamura, Hajime / Yodoi, Junji

IUBMB life

2008 Volume 60, Issue 10, Page(s) 656–660

Abstract: Thioredoxin (TRX) is a 12-kDa protein with redox-active dithiol in the active site -Cys-Gly-Pro-Cys- and constitutes a major thiol reducing system. TRX protects cells from stress-induced damage through antioxidative, antiapoptotic, and anti-inflammatory ... ...

Abstract	Thioredoxin (TRX) is a 12-kDa protein with redox-active dithiol in the active site -Cys-Gly-Pro-Cys- and constitutes a major thiol reducing system. TRX protects cells from stress-induced damage through antioxidative, antiapoptotic, and anti-inflammatory effect. In animal models, thioacetamide (TAA)-induced acute hepatitis and TAA-induced liver fibrosis was attenuated in TRX transgenic (TRXTG) mice. Plasma level of TRX is a good marker for hepatitis and nonalcoholic steatohepatitis (NASH) in human patients. Recently, we identified TRX binding protein 2 (TBP2) in a yeast two-hybrid screening. TBP2 regulates both the expression and reducing activity of TRX as well as cell growth. TBP2 knockout (TBP2KO) mice showed disorder in lipid metabolism. TBP2 plays a multiple role on cell growth and lipid and glucose metabolism. Thus, TRX and TBP2 play important roles in the pathophysiology of liver diseases, including NASH, indicating that ratio of TRX and TBP2 expression could be a novel marker of liver diseases like NASH.
MeSH term(s)	Animals ; Antioxidants/metabolism ; Carrier Proteins/metabolism ; Humans ; Liver/cytology ; Liver/metabolism ; Liver/pathology ; Oxidation-Reduction ; Thioredoxins/metabolism
Chemical Substances	Antioxidants ; Carrier Proteins ; TXNIP protein, human ; Thioredoxins (52500-60-4)
Language	English
Publishing date	2008-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1492141-8
ISSN	1521-6551 ; 1521-6543
ISSN (online)	1521-6551
ISSN	1521-6543
DOI	10.1002/iub.102
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Article ; Online: Downregulation of cardiac lineage protein-1 confers cardioprotection through the upregulation of redox effectors.

Gurusamy, Narasimman / Lekli, Istvan / Ahsan, Md Kaimul / Ray, Diptarka / Mukherjee, Subhendu / Mascareno, Eduardo / Siddiqui, M A Q / Das, Dipak K

FEBS letters

2010 Volume 584, Issue 1, Page(s) 187–193

Abstract: CLP-1, the mouse homologue of human Hexim1 protein, exerts inhibitory control on transcriptional elongation factor-b of RNA transcript elongation. Previously, we have demonstrated that downregulation of cardiac lineage protein-1 (CLP-1) in CLP-1(+/-) ... ...

Abstract	CLP-1, the mouse homologue of human Hexim1 protein, exerts inhibitory control on transcriptional elongation factor-b of RNA transcript elongation. Previously, we have demonstrated that downregulation of cardiac lineage protein-1 (CLP-1) in CLP-1(+/-) heterozygous mice affords cardioprotection against ischemia-reperfusion injury. Our current study results show that the improvement in cardiac function in CLP-1(+/-) mice after ischemia-reperfusion injury is achieved through the potentiation of redox signaling and their molecular targets including redox effector factor-1, nuclear factor erythroid 2-related factor, and NADPH oxidase 4 and the active usage of thioredoxin-1, thioredoxin-2, glutaredoxin-1 and glutaredoxin-2. Our results suggest that drugs designed to down regulate CLP-1 could confer cardioprotection through the potentiation of redox cycling.
MeSH term(s)	Animals ; Cardiotonic Agents/chemistry ; Cardiotonic Agents/pharmacology ; Cytoprotection ; DNA-(Apurinic or Apyrimidinic Site) Lyase/metabolism ; Down-Regulation ; Drug Design ; Glutaredoxins/metabolism ; Heterozygote ; Mice ; Mice, Mutant Strains ; NADPH Oxidase 4 ; NADPH Oxidases/metabolism ; NF-E2 Transcription Factor/metabolism ; Reperfusion Injury/genetics ; Reperfusion Injury/metabolism ; Thioredoxins/metabolism ; Transcription Factors/antagonists & inhibitors ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Up-Regulation
Chemical Substances	Cardiotonic Agents ; Glutaredoxins ; Hexim1 protein, mouse ; NF-E2 Transcription Factor ; Transcription Factors ; Thioredoxins (52500-60-4) ; NADPH Oxidase 4 (EC 1.6.3.-) ; NADPH Oxidases (EC 1.6.3.-) ; Nox4 protein, mouse (EC 1.6.3.-) ; Apex1 protein, mouse (EC 4.2.99.18) ; DNA-(Apurinic or Apyrimidinic Site) Lyase (EC 4.2.99.18)
Language	English
Publishing date	2010-01-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1016/j.febslet.2009.11.054
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Article ; Online: Thioredoxin-binding protein-2 deficiency enhances methionine-choline deficient diet-induced hepatic steatosis but inhibits steatohepatitis in mice.

Ahsan, Md Kaimul / Okuyama, Hiroaki / Hoshino, Yuma / Oka, Shin-Ichi / Masutani, Hiroshi / Yodoi, Junji / Nakamura, Hajime

Antioxidants & redox signaling

2009 Volume 11, Issue 10, Page(s) 2573–2584

Abstract: In nonalcoholic fatty liver disease, oxidative stress is believed to play a crucial role as a second-hit for the progression of simple steatosis to steatohepatitis. Thioredoxin (TRX) is a potent antioxidant molecule that exerts anti-apoptotic and anti- ... ...

Abstract	In nonalcoholic fatty liver disease, oxidative stress is believed to play a crucial role as a second-hit for the progression of simple steatosis to steatohepatitis. Thioredoxin (TRX) is a potent antioxidant molecule that exerts anti-apoptotic and anti-inflammatory functions. TRX-binding protein-2 (TBP-2) is an endogenous negative regulator of TRX. Deficiency of TBP-2 in mice causes hyperlipidemia, hepatic steatosis, hypoglycemia, and bleeding tendency, resembling Reye syndrome in a fasting/glucose-deficient state. The aim of this study was to investigate the role of TBP-2 in the development of nonalcoholic steatohepatitis (NASH). TBP-2-deficient (TBP-2(-/-)) and wild-type (WT) mice were fed either a normal or methionine-choline-deficient (MCD) diet for up to 10 weeks. Compared with WT mice, TBP-2(-/-) mice showed severe simple steatosis rather than steatohepatitis. However, oxidative stress determined by lipid peroxidation and DNA damage, neutrophil infiltration, and hepatic fibrosis were attenuated in TBP-2(-/-) mice. PCR analysis showed the expressions of fibrosis-inducing and inflammatory cytokine-related genes were less in TBP-2(-/-) mice. Moreover, leptin, SREBP1c, PPARgamma, and adipogenesis-lipogenesis-related genes were upregulated in TBP-2(-/-) mice. These results strongly suggested that TBP-2 might be involved in pathogenesis of NASH in WT mice, and inhibitors of TBP-2 could be useful in the prevention or treatment of NASH.
MeSH term(s)	Animals ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Choline Deficiency/metabolism ; Diet ; Fatty Liver/etiology ; Fatty Liver/metabolism ; Fatty Liver/pathology ; Female ; Fibrosis/metabolism ; Fibrosis/pathology ; Hepatitis/etiology ; Hepatitis/metabolism ; Hepatitis/pathology ; Interferon-gamma/genetics ; Interferon-gamma/metabolism ; Interleukin-1beta/genetics ; Interleukin-1beta/metabolism ; Liver/cytology ; Liver/metabolism ; Liver/pathology ; Male ; Methionine/deficiency ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; NF-kappa B/genetics ; NF-kappa B/metabolism ; Neutrophils/cytology ; Neutrophils/metabolism ; Oxidative Stress ; Thioredoxins/genetics ; Thioredoxins/metabolism ; Triglycerides/blood ; Tumor Necrosis Factor-alpha/genetics ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	Carrier Proteins ; Interleukin-1beta ; NF-kappa B ; Triglycerides ; Tumor Necrosis Factor-alpha ; Txnip protein, mouse ; Thioredoxins (52500-60-4) ; Interferon-gamma (82115-62-6) ; Methionine (AE28F7PNPL)
Language	English
Publishing date	2009-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2009.2385
Database	MEDical Literature Analysis and Retrieval System OnLINE

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