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Article: Substance P failed to reverse dextran sulfate sodium-induced murine colitis mediated by mitochondrial dysfunction: implications in ulcerative colitis.

Chandraiah, Spoorthi B / Ghosh, Shashwati / Saha, Ishita / More, Sunil S / Annappa, Gautham S / Maiti, Arpan K

2021 Volume 11, Issue 4, Page(s) 199

Abstract: As controversy exists about the efficacy of substance P (SP) in treating ulcerative colitis (UC) with no previous study highlighting the impact of SP on mitochondrial dysfunction in this diseased condition, it became logical to perform the present study. ...

Abstract	As controversy exists about the efficacy of substance P (SP) in treating ulcerative colitis (UC) with no previous study highlighting the impact of SP on mitochondrial dysfunction in this diseased condition, it became logical to perform the present study. C57BL/6 J mice were administered with DSS @ 3.5%/gm body weight for 3 cycles of 5 days each followed by i.v. dose of SP @ 5nmole per kg for consecutive 7 days. Histopathological features were noticed in the affected colon along with colonic mitochondrial dysfunction, alterations in mitochondrial stress variables and enhanced colonic cell death. Interestingly, SP failed to reverse colitic features and proved ineffective in inhibiting mitochondrial dysfunction. Unexpectedly SP alone seemed to impart detrimental effects on some of the mitochondrial functions, enhanced lipid peroxidation and increased staining intensities for caspases 3 and 9 in the normal colon. To substantiate in vivo findings and to assess free radical scavenging property of SP, Caco-2 cells were exposed to DSS with or without SP in the presence and absence of specific free radical scavengers and antioxidants. Interestingly, in vitro treatment with SP failed to restore mitochondrial functions and its efficacy proved below par compared to SOD and DMSO indicating involvement of O
Language	English
Publishing date	2021-03-29
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2600522-0
ISSN	2190-5738 ; 2190-572X
ISSN (online)	2190-5738
ISSN	2190-572X
DOI	10.1007/s13205-021-02755-2
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Article: Substance P failed to reverse dextran sulfate sodium-induced murine colitis mediated by mitochondrial dysfunction: implications in ulcerative colitis

Chandraiah, Spoorthi B / Ghosh, Shashwati / Saha, Ishita / More, Sunil S / Annappa, Gautham S / Maiti, Arpan K

3 Biotech. 2021 Apr., v. 11, no. 4

2021

Abstract	As controversy exists about the efficacy of substance P (SP) in treating ulcerative colitis (UC) with no previous study highlighting the impact of SP on mitochondrial dysfunction in this diseased condition, it became logical to perform the present study. C57BL/6 J mice were administered with DSS @ 3.5%/gm body weight for 3 cycles of 5 days each followed by i.v. dose of SP @ 5nmole per kg for consecutive 7 days. Histopathological features were noticed in the affected colon along with colonic mitochondrial dysfunction, alterations in mitochondrial stress variables and enhanced colonic cell death. Interestingly, SP failed to reverse colitic features and proved ineffective in inhibiting mitochondrial dysfunction. Unexpectedly SP alone seemed to impart detrimental effects on some of the mitochondrial functions, enhanced lipid peroxidation and increased staining intensities for caspases 3 and 9 in the normal colon. To substantiate in vivo findings and to assess free radical scavenging property of SP, Caco-2 cells were exposed to DSS with or without SP in the presence and absence of specific free radical scavengers and antioxidants. Interestingly, in vitro treatment with SP failed to restore mitochondrial functions and its efficacy proved below par compared to SOD and DMSO indicating involvement of O₂•⁻ and •OH in the progression of UC. Besides, catalase, L-NAME and MEG proved ineffective indicating non-involvement of H₂O₂, NO and ONOO⁻ in UC. Thus, SP may not be a potent anti-colitogenic agent targeting colonic mitochondrial dysfunction for maintenance of colon epithelial tract as it lacks free radical scavenging property.
Keywords	body weight ; caspases ; catalase ; cell death ; colon ; dextran sulfate ; epithelium ; free radicals ; histopathology ; lipid peroxidation ; mice ; mitochondria ; substance P ; ulcerative colitis
Language	English
Dates of publication	2021-04
Size	p. 199.
Publishing place	Springer International Publishing
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	2600522-0
ISSN	2190-5738 ; 2190-572X
ISSN (online)	2190-5738
ISSN	2190-572X
DOI	10.1007/s13205-021-02755-2
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Colonic levels of vasoactive intestinal peptide decrease during infection and exogenous VIP protects epithelial mitochondria against the negative effects of IFNγ and TNFα induced during Citrobacter rodentium infection.

Maiti, Arpan K / Sharba, Sinan / Navabi, Nazanin / Lindén, Sara K

PloS one

2018 Volume 13, Issue 9, Page(s) e0204567

Abstract: Citrobacter rodentium infection is a model for infection with attaching and effacing pathogens, such as enteropathogenic Escherichia coli. The vasoactive intestinal peptide (VIP) has emerged as an anti-inflammatory agent, documented to inhibit Th1 immune ...

Abstract	Citrobacter rodentium infection is a model for infection with attaching and effacing pathogens, such as enteropathogenic Escherichia coli. The vasoactive intestinal peptide (VIP) has emerged as an anti-inflammatory agent, documented to inhibit Th1 immune responses and successfully treat animal models of inflammation. VIP is also a mucus secretagogue. Here, we found that colonic levels of VIP decrease during murine C. rodentium infection with a similar time dependency as measurements reflecting mitochondrial function and epithelial integrity. The decrease in VIP appears mainly driven by changes in the cytokine environment, as no changes in VIP levels were detected in infected mice lacking interferon gamma (IFNγ). VIP supplementation alleviated the reduction of activity and levels of mitochondrial respiratory complexes I and IV, mitochondrial phosphorylation capacity, transmembrane potential and ATP generation caused by IFNγ, TNFα and C. rodentium infection, in an in vitro mucosal surface. Similarly, VIP treatment regimens that included the day 5-10 post infection period alleviated decreases in enzyme complexes I and IV, phosphorylation capacity, mitochondrial transmembrane potential and ATP generation as well as increased apoptosis levels during murine infection with C. rodentium. However, VIP treatment failed to alleviate colitis, although there was a tendency to decreased pathogen density in contact with the epithelium and in the spleen. Both in vivo and in vitro, NO generation increased during C. rodentium infection, which was alleviated by VIP. Thus, therapeutic VIP administration to restore the decreased levels during infection had beneficial effects on epithelial cells and their mitochondria, but not on the overall infection outcome.
MeSH term(s)	Animals ; Citrobacter rodentium/pathogenicity ; Colitis/drug therapy ; Colitis/immunology ; Colitis/metabolism ; Colon/immunology ; Colon/metabolism ; Disease Models, Animal ; Electron Transport Complex I/metabolism ; Electron Transport Complex IV/metabolism ; Enterobacteriaceae Infections/drug therapy ; Enterobacteriaceae Infections/immunology ; Enterobacteriaceae Infections/metabolism ; HT29 Cells ; Host Microbial Interactions ; Humans ; Interferon-gamma/metabolism ; Intestinal Mucosa/immunology ; Intestinal Mucosa/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondria/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Vasoactive Intestinal Peptide/administration & dosage ; Vasoactive Intestinal Peptide/immunology ; Vasoactive Intestinal Peptide/metabolism
Chemical Substances	Tumor Necrosis Factor-alpha ; Vasoactive Intestinal Peptide (37221-79-7) ; Interferon-gamma (82115-62-6) ; Electron Transport Complex I (EC 1.6.5.3) ; Electron Transport Complex IV (EC 1.9.3.1)
Language	English
Publishing date	2018-09-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0204567
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Article: Enhancement in cellular Na+K+ATPase activity by low doses of peroxynitrite in mouse renal tissue and in cultured HK2 cells.

Maiti, Arpan K / Islam, Mohammed T / Satou, Ryousuke / Majid, Dewan S A

Physiological reports

2016 Volume 4, Issue 7

Abstract: In the normal condition, endogenous formation of peroxynitrite (ONOO-) from the interaction of nitric oxide and superoxide has been suggested to play a renoprotective role. However, the exact mechanism associated with renoprotection by this radical ... ...

Abstract	In the normal condition, endogenous formation of peroxynitrite (ONOO-) from the interaction of nitric oxide and superoxide has been suggested to play a renoprotective role. However, the exact mechanism associated with renoprotection by this radical compound is not yet clearly defined. AlthoughONOO- usually inhibits renal tubular Na(+)K(+)ATPase (NKA) activity at high concentrations (micromolar to millimolar range [μM-mM], achieved in pathophysiological conditions), the effects at lower concentrations (nanomolar range [nM], relevant in normal condition) remain unknown. To examine the direct effect ofONOO- onNKAactivity, preparations of cellular membrane fraction from mouse renal tissue and from culturedHK2 cells (human proximal tubular epithelial cell lines) were incubated for 10 and 30 min each with different concentrations ofONOO- (10 nmol/L-200 μmol/L).NKAactivity in these samples (n = 5 in each case) was measured via a colorimetric assay capable of detecting inorganic phosphate. At high concentrations (1-200 μmol/L),ONOO- caused dose-dependent inhibition ofNKAactivity (-3.0 ± 0.6% and -36.4 ± 1.4%). However,NKAactivity remained unchanged at 100 and 500 nmol/LONOO- concentration, but interestingly, at lower concentrations (10 and 50 nmol/L),ONOO- caused small but significant increases in theNKAactivity (3.3 ± 1.1% and 3.1 ± 0.6%). Pretreatment with aONOO- scavenger, mercaptoethylguanidine (MEG; 200 μmol/L), prevented these biphasic responses toONOO-. This dose-dependent biphasic action ofONOO(-)onNKAactivity may implicate that this radical compound helps to maintain sodium homeostasis either by enhancing tubular sodium reabsorption under normal conditions or by inhibiting it during oxidative stress conditions.
MeSH term(s)	Animals ; Cell Line ; Cell Membrane/drug effects ; Cell Membrane/enzymology ; Dose-Response Relationship, Drug ; Enzyme Activators/pharmacology ; Enzyme Inhibitors/pharmacology ; Epithelial Cells/drug effects ; Epithelial Cells/enzymology ; Free Radical Scavengers/pharmacology ; Humans ; Kidney Tubules, Proximal/drug effects ; Kidney Tubules, Proximal/enzymology ; Mice, Inbred C57BL ; Nitric Oxide/metabolism ; Peroxynitrous Acid/pharmacology ; Sodium-Potassium-Exchanging ATPase/antagonists & inhibitors ; Sodium-Potassium-Exchanging ATPase/metabolism ; Time Factors
Chemical Substances	Enzyme Activators ; Enzyme Inhibitors ; Free Radical Scavengers ; Peroxynitrous Acid (14691-52-2) ; Nitric Oxide (31C4KY9ESH) ; Sodium-Potassium-Exchanging ATPase (EC 7.2.2.13)
Language	English
Publishing date	2016-04-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2724325-4
ISSN	2051-817X
ISSN	2051-817X
DOI	10.14814/phy2.12766
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Article ; Online: IL-4 Protects the Mitochondria Against TNFα and IFNγ Induced Insult During Clearance of Infection with Citrobacter rodentium and Escherichia coli.

Maiti, Arpan K / Sharba, Sinan / Navabi, Nazanin / Forsman, Huamei / Fernandez, Harvey R / Lindén, Sara K

Scientific reports

2015 Volume 5, Page(s) 15434

Abstract: Citrobacter rodentium is a murine pathogen that serves as a model for enteropathogenic Escherichia coli. C. rodentium infection reduced the quantity and activity of mitochondrial respiratory complexes I and IV, as well as phosphorylation capacity, ... ...

Abstract	Citrobacter rodentium is a murine pathogen that serves as a model for enteropathogenic Escherichia coli. C. rodentium infection reduced the quantity and activity of mitochondrial respiratory complexes I and IV, as well as phosphorylation capacity, mitochondrial transmembrane potential and ATP generation at day 10, 14 and 19 post infection. Cytokine mRNA quantification showed increased levels of IFNγ, TNFα, IL-4, IL-6, and IL-12 during infection. The effects of adding these cytokines, C. rodentium and E. coli were hence elucidated using an in vitro colonic mucosa. Both infection and TNFα, individually and combined with IFNγ, decreased complex I and IV enzyme levels and mitochondrial function. However, IL-4 reversed these effects, and IL-6 protected against loss of complex IV. Both in vivo and in vitro, the dysfunction appeared caused by nitric oxide-generation, and was alleviated by an antioxidant targeting mitochondria. IFNγ -/- mice, containing a similar pathogen burden but higher IL-4 and IL-6, displayed no loss of any of the four complexes. Thus, the cytokine environment appears to be a more important determinant of mitochondrial function than direct actions of the pathogen. As IFNγ and TNFα levels increase during clearance of infection, the concomitant increase in IL-4 and IL-6 protects mitochondrial function.
MeSH term(s)	Adenosine Triphosphate/biosynthesis ; Animals ; Caspase 3/metabolism ; Cell Death ; Citrobacter rodentium ; Colitis/genetics ; Colitis/metabolism ; Colitis/microbiology ; Colitis/pathology ; Cytokines/genetics ; Cytokines/metabolism ; Disease Models, Animal ; Electron Transport Chain Complex Proteins/metabolism ; Enterobacteriaceae Infections/genetics ; Enterobacteriaceae Infections/metabolism ; Enterobacteriaceae Infections/microbiology ; Enterobacteriaceae Infections/pathology ; Enzyme Activation ; Escherichia coli ; Interferon-gamma/genetics ; Interferon-gamma/metabolism ; Interleukin-4/metabolism ; Membrane Potential, Mitochondrial ; Mice ; Mice, Knockout ; Mitochondria/drug effects ; Mitochondria/metabolism ; Nitric Oxide/metabolism ; Organophosphorus Compounds/pharmacology ; Phosphorylation ; Tumor Necrosis Factor-alpha/metabolism ; Ubiquinone/analogs & derivatives ; Ubiquinone/pharmacology
Chemical Substances	Cytokines ; Electron Transport Chain Complex Proteins ; Organophosphorus Compounds ; Tumor Necrosis Factor-alpha ; Ubiquinone (1339-63-5) ; Interleukin-4 (207137-56-2) ; Nitric Oxide (31C4KY9ESH) ; mitoquinone (47BYS17IY0) ; Interferon-gamma (82115-62-6) ; Adenosine Triphosphate (8L70Q75FXE) ; Caspase 3 (EC 3.4.22.-)
Language	English
Publishing date	2015-10-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/srep15434
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Article ; Online: Quinone and oxyradical scavenging properties of N-acetylcysteine prevent dopamine mediated inhibition of Na+, K+-ATPase and mitochondrial electron transport chain activity in rat brain: implications in the neuroprotective therapy of Parkinson's disease.

Bagh, Maria B / Maiti, Arpan K / Jana, Sirsendu / Banerjee, Kalpita / Roy, Arun / Chakrabarti, Sasanka

Free radical research

2008 Volume 42, Issue 6, Page(s) 574–581

Abstract: Dopamine oxidation products such as H2O2 and reactive quinones have been held responsible for various toxic actions of dopamine, which have implications in the aetiopathogenesis of Parkinson's disease. This study has shown that N-acetylcysteine (0.25-1 ... ...

Abstract	Dopamine oxidation products such as H2O2 and reactive quinones have been held responsible for various toxic actions of dopamine, which have implications in the aetiopathogenesis of Parkinson's disease. This study has shown that N-acetylcysteine (0.25-1 mm) is a potent scavenger of both H2O2 and toxic quinones derived from dopamine and it further prevents dopamine mediated inhibition of Na+,K+-ATPase activity and mitochondrial respiratory chain function. The quinone scavenging ability of N-acetylcysteine is presumably related to its protective effect against dopamine mediated inhibition of mitochondrial respiratory chain activity. However, both H2O2 scavenging and quinone scavenging properties of N-acetylcysteine probably account for its protective effect against Na+,K+-ATPase inhibition induced by dopamine. The results have important implications in the neuroprotective therapy of sporadic Parkinson's disease since inactivation of mitochondrial respiratory activity and Na+,K+-ATPase may trigger intracellular damage pathways leading to the death of nigral dopaminergic neurons.
MeSH term(s)	Acetylcysteine/pharmacology ; Adenosine Triphosphate/chemistry ; Animals ; Benzoquinones/chemistry ; Brain/metabolism ; Disease Models, Animal ; Dopamine/metabolism ; Free Radical Scavengers/pharmacology ; Free Radicals ; Humans ; Hydrogen Peroxide/metabolism ; Mitochondria/metabolism ; Parkinson Disease/metabolism ; Parkinson Disease/pathology ; Rats ; Sodium-Potassium-Exchanging ATPase/chemistry ; Sodium-Potassium-Exchanging ATPase/physiology
Chemical Substances	Benzoquinones ; Free Radical Scavengers ; Free Radicals ; quinone (3T006GV98U) ; Adenosine Triphosphate (8L70Q75FXE) ; Hydrogen Peroxide (BBX060AN9V) ; Sodium-Potassium-Exchanging ATPase (EC 3.6.3.9) ; Dopamine (VTD58H1Z2X) ; Acetylcysteine (WYQ7N0BPYC)
Language	English
Publishing date	2008-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1194130-3
ISSN	1029-2470 ; 1071-5762
ISSN (online)	1029-2470
ISSN	1071-5762
DOI	10.1080/10715760802158430
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Article: Epidermal growth factor receptor and proliferating cell nuclear antigen in astrocytomas.

Maiti, Arpan K / Ghosh, Keya / Chatterjee, Uttara / Chakrobarti, Sasanka / Chatterjee, Sandip / Basu, Samik

Neurology India

2008 Volume 56, Issue 4, Page(s) 456–462

Abstract: Aims: The involvement of various growth factors, growth factor receptors and proliferative markers in the molecular pathogenesis of astrocytic neoplasms are being studied extensively. Epidermal Growth Factor Receptor (EGFR) gene overexpression occurs in ...

Abstract	Aims: The involvement of various growth factors, growth factor receptors and proliferative markers in the molecular pathogenesis of astrocytic neoplasms are being studied extensively. Epidermal Growth Factor Receptor (EGFR) gene overexpression occurs in nearly 50% of cases of glioblastoma. Since EGFR and proliferating cell nuclear antigen (PCNA) are involved in mitogenic signal transduction and cellular proliferation pathway, we have studied the correlation between the expression of EGFR and PCNA labeling index in astrocytic tumors. Materials and methods: We investigated the immunohistochemical expression of EGFR and PCNA using the appropriate monoclonal antibodies in 40 cases of astrocytic tumors of which 21 cases were glioblastoma, eight cases were Grade III or anaplastic astrocytomas and six cases were Grade II or diffuse astrocytomas and five cases were Grade I or pilocytic astrocytomas. Results: Both the EGFR expression and PCNA labeling index increase with increasing grades of astrocytomas with a significantly high percentage of cells showing positive staining for both EGFR and PCNA in GBM and Grade III astrocytomas compared to Grade II astrocytomas. The expression levels of both EGFR and PCNA were low in Grade I or pilocytic astrocytomas. Conclusions: A significant correlation was found between EGFR overexpression and PCNA labeling index in Grade III and Grade II astrocytomas and glioblastoma. These suggest that the tumor proliferation, at least in higher grades of astrocytomas is dependent in some measure on EGF and EGFR-related signaling pathways.
MeSH term(s)	Adult ; Aged ; Astrocytoma/genetics ; Astrocytoma/metabolism ; Brain Neoplasms/genetics ; Brain Neoplasms/metabolism ; ErbB Receptors/genetics ; ErbB Receptors/metabolism ; Female ; Humans ; Immunohistochemistry ; Male ; Middle Aged ; Proliferating Cell Nuclear Antigen/genetics ; Proliferating Cell Nuclear Antigen/metabolism
Chemical Substances	Proliferating Cell Nuclear Antigen ; ErbB Receptors (EC 2.7.10.1)
Language	English
Publishing date	2008-12-31
Publishing country	India
Document type	Journal Article
ZDB-ID	415522-1
ISSN	1998-4022 ; 0028-3886
ISSN (online)	1998-4022
ISSN	0028-3886
DOI	10.4103/0028-3886.44827
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Substance P failed to reverse dextran sulfate sodium-induced murine colitis mediated by mitochondrial dysfunction: implications in ulcerative colitis.

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Article: Substance P failed to reverse dextran sulfate sodium-induced murine colitis mediated by mitochondrial dysfunction: implications in ulcerative colitis

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Article ; Online: Colonic levels of vasoactive intestinal peptide decrease during infection and exogenous VIP protects epithelial mitochondria against the negative effects of IFNγ and TNFα induced during Citrobacter rodentium infection.

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Article: Enhancement in cellular Na+K+ATPase activity by low doses of peroxynitrite in mouse renal tissue and in cultured HK2 cells.

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Article ; Online: IL-4 Protects the Mitochondria Against TNFα and IFNγ Induced Insult During Clearance of Infection with Citrobacter rodentium and Escherichia coli.

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Article ; Online: Quinone and oxyradical scavenging properties of N-acetylcysteine prevent dopamine mediated inhibition of Na+, K+-ATPase and mitochondrial electron transport chain activity in rat brain: implications in the neuroprotective therapy of Parkinson's disease.

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Article: Epidermal growth factor receptor and proliferating cell nuclear antigen in astrocytomas.

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