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Article ; Online: Kidney atrophy vs hypertrophy in diabetes: which cells are involved?

Habib, Samy L

2018 Volume 17, Issue 14, Page(s) 1683–1687

Abstract: One of the first structural changes in diabetic nephropathy (DN) is the renal enlargement. These changes resulted in renal hypertrophy in both glomerular and tubular cells. Shrink in the kidney size, which described as kidney atrophy resulted from the ... ...

Abstract	One of the first structural changes in diabetic nephropathy (DN) is the renal enlargement. These changes resulted in renal hypertrophy in both glomerular and tubular cells. Shrink in the kidney size, which described as kidney atrophy resulted from the loss of nephrons or abnormal nephron function and lead to loss of the kidney function. On the other hand, increase in kidney size, which described as hypertrophy resulted from increase in proximal tubular epithelial and glomerular cells size. However overtime, tubular atrophy and tubulointerstitial fibrosis occurs as subsequent changes in tubular cell hypertrophy, which is associated with the infiltration of fibroblast cells into the tubulointerstitial space. The rate of deterioration of kidney function shows a strong correlation with the degree of tubulointerstitial fibrosis. A consequence of long-standing diabetes/hyperglycemia may lead to major changes in renal structure that occur but not specific only to nephropathy. Identifying type of cells that involves in renal atrophy and hypertrophy may help to find a therapeutic target to treat diabetic nephropathy. In summary, the early changes in diabetic kidney are mainly includes the increase in tubular basement membrane thickening which lead to renal hypertrophy. On the other hand, only renal tubule is subjected to apoptosis, which is one of the characteristic morphologic changes in diabetic kidney to form tubular atrophy at the late stage of diabetes.
MeSH term(s)	Animals ; Atrophy ; Diabetic Nephropathies/pathology ; Humans ; Hypertrophy ; Kidney/pathology
Language	English
Publishing date	2018-07-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
DOI	10.1080/15384101.2018.1496744
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Tuberin in renal cell hypertrophy.

Habib, Samy L

Cell cycle (Georgetown, Tex.)

2014 Volume 13, Issue 6, Page(s) 869–870

MeSH term(s)	Animals ; Diabetic Nephropathies/metabolism ; Fibronectins/biosynthesis ; Male ; Tumor Suppressor Proteins/deficiency
Chemical Substances	Fibronectins ; Tumor Suppressor Proteins
Language	English
Publishing date	2014-02-03
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
DOI	10.4161/cc.27942
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Article ; Online: A novel role of snail in regulating tuberin/AMPK pathways to promote renal fibrosis in the new mouse model of type II diabetes.

Liang, Sitai / Yadav, Mukesh / Vogel, Kristine S / Habib, Samy L

FASEB bioAdvances

2021 Volume 3, Issue 9, Page(s) 730–743

Abstract: Epithelial-mesenchymal transition (EMT) plays an important role in tissue fibrosis following chronic exposure to hyperglycemia. This study investigates the role of chronic diabetes in regulating tuberin/snail/AMPK to enhance EMT and increase renal ... ...

Abstract	Epithelial-mesenchymal transition (EMT) plays an important role in tissue fibrosis following chronic exposure to hyperglycemia. This study investigates the role of chronic diabetes in regulating tuberin/snail/AMPK to enhance EMT and increase renal fibrosis. A new mouse model of db/db/
Language	English
Publishing date	2021-07-08
Publishing country	United States
Document type	Journal Article
ISSN	2573-9832
ISSN (online)	2573-9832
DOI	10.1096/fba.2020-00134
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Article: Role of Base Excision Repair in Innate Immune Cells and Its Relevance for Cancer Therapy.

Zhao, Shengyuan / Habib, Samy L / Senejani, Alireza G / Sebastian, Manu / Kidane, Dawit

Biomedicines

2022 Volume 10, Issue 3

Abstract: Innate immunity is critical for immediate recognition and elimination of invading pathogens or defense against cancer cell growth. Dysregulation of innate immune systems is associated with the pathogenesis of different types of inflammatory diseases, ... ...

Abstract	Innate immunity is critical for immediate recognition and elimination of invading pathogens or defense against cancer cell growth. Dysregulation of innate immune systems is associated with the pathogenesis of different types of inflammatory diseases, including cancer. In addition, the maintenance of innate immune cells' genomic integrity is crucial for the survival of all organisms. Oxidative stress generated from innate immune cells may cause self-inflicted DNA base lesions as well as DNA damage on others neighboring cells, including cancer cells. Oxidative DNA base damage is predominantly repaired by base excision repair (BER). BER process different types of DNA base lesions that are presented in cancer and innate immune cells to maintain genomic integrity. However, mutations in BER genes lead to impaired DNA repair function and cause insufficient genomic integrity. Moreover, several studies have implicated that accumulation of DNA damage leads to chromosomal instability that likely activates the innate immune signaling. Furthermore, dysregulation of BER factors in cancer cells modulate the infiltration of innate immune cells to the tumor microenvironment. In the current review, the role of BER in cancer and innate immune cells and its impact on innate immune signaling within the tumor microenvironment is summarized. This is a special issue that focuses on DNA damage and cancer therapy to demonstrate how BER inhibitor or aberrant repair modulates innate inflammatory response and impact immunotherapy approaches. Overall, the review provides substantial evidence to understand the impact of BER in innate immune response dynamics within the current immune-based therapeutic strategy.
Language	English
Publishing date	2022-02-26
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines10030557
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Article ; Online: TP63 Is Significantly Upregulated in Diabetic Kidney.

Liang, Sitai / Nayak, Bijaya K / Vogel, Kristine S / Habib, Samy L

International journal of molecular sciences

2021 Volume 22, Issue 8

Abstract: The role of tumor protein 63 (TP63) in regulating insulin receptor substrate 1 (IRS-1) and other downstream signal proteins in diabetes has not been characterized. RNAs extracted from kidneys of diabetic mice (db/db) were sequenced to identify genes that ...

Abstract	The role of tumor protein 63 (TP63) in regulating insulin receptor substrate 1 (IRS-1) and other downstream signal proteins in diabetes has not been characterized. RNAs extracted from kidneys of diabetic mice (db/db) were sequenced to identify genes that are involved in kidney complications. RNA sequence analysis showed more than 4- to 6-fold increases in TP63 expression in the diabetic mice's kidneys, compared to wild-type mice at age 10 and 12 months old. In addition, the kidneys from diabetic mice showed significant increases in TP63 mRNA and protein expression compared to WT mice. Mouse proximal tubular cells exposed to high glucose (HG) for 48 h showed significant decreases in IRS-1 expression and increases in TP63, compared to cells grown in normal glucose (NG). When TP63 was downregulated by siRNA, significant increases in IRS-1 and activation of AMP-activated protein kinase (AMPK (p-AMPK-Th
MeSH term(s)	Adenylate Kinase/metabolism ; Aminoimidazole Carboxamide/analogs & derivatives ; Aminoimidazole Carboxamide/pharmacology ; Animals ; Blood Glucose/metabolism ; Cells, Cultured ; Diabetes Mellitus, Experimental/blood ; Diabetes Mellitus, Experimental/genetics ; Diabetic Nephropathies/blood ; Diabetic Nephropathies/genetics ; Down-Regulation/drug effects ; Down-Regulation/genetics ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Insulin Receptor Substrate Proteins/genetics ; Insulin Receptor Substrate Proteins/metabolism ; Kidney Tubules, Proximal/pathology ; Models, Biological ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Ribonucleotides/pharmacology ; Signal Transduction/drug effects ; Trans-Activators/genetics ; Trans-Activators/metabolism ; Tuberous Sclerosis Complex 2 Protein/pharmacology ; Up-Regulation/drug effects ; Up-Regulation/genetics
Chemical Substances	Blood Glucose ; Hif1a protein, mouse ; Hypoxia-Inducible Factor 1, alpha Subunit ; Insulin Receptor Substrate Proteins ; Irs1 protein, mouse ; RNA, Messenger ; Ribonucleotides ; Trans-Activators ; Trp63 protein, mouse ; Tuberous Sclerosis Complex 2 Protein ; Aminoimidazole Carboxamide (360-97-4) ; Adenylate Kinase (EC 2.7.4.3) ; AICA ribonucleotide (F0X88YW0YK)
Language	English
Publishing date	2021-04-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22084070
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Article: Diabetes and renal tubular cell apoptosis.

Habib, Samy L

World journal of diabetes

2013 Volume 4, Issue 2, Page(s) 27–30

Abstract: Apoptosis contributes to the development of diabetic nephropathy, but the mechanism by which high glucose induces apoptosis is not fully understood. Apoptosis of tubular epithelial cells is a major feature of diabetic kidney disease, and hyperglycemia ... ...

Abstract	Apoptosis contributes to the development of diabetic nephropathy, but the mechanism by which high glucose induces apoptosis is not fully understood. Apoptosis of tubular epithelial cells is a major feature of diabetic kidney disease, and hyperglycemia triggers the generation of free radicals and oxidant stress in tubular cells. Hyperglycemia and high glucose in vitro also lead to apoptosis, a form of programmed cell death. High glucose similar to those seen with hyperglycemia in people with diabetes mellitus, lead to accelerated apoptosis, a form of programmed cell death characterized by cell shrinkage, chromatin condensation and DNA fragmentation, in variety of cell types, including renal proximal tubular epithelial cells.
Language	English
Publishing date	2013-02-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	2583471-X
ISSN	1948-9358
ISSN	1948-9358
DOI	10.4239/wjd.v4.i2.27
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Article ; Online: Role of Base Excision Repair in Innate Immune Cells and Its Relevance for Cancer Therapy

Shengyuan Zhao / Samy L. Habib / Alireza G. Senejani / Manu Sebastian / Dawit Kidane

Biomedicines, Vol 10, Iss 557, p

2022 Volume 557

Abstract	Innate immunity is critical for immediate recognition and elimination of invading pathogens or defense against cancer cell growth. Dysregulation of innate immune systems is associated with the pathogenesis of different types of inflammatory diseases, including cancer. In addition, the maintenance of innate immune cells’ genomic integrity is crucial for the survival of all organisms. Oxidative stress generated from innate immune cells may cause self-inflicted DNA base lesions as well as DNA damage on others neighboring cells, including cancer cells. Oxidative DNA base damage is predominantly repaired by base excision repair (BER). BER process different types of DNA base lesions that are presented in cancer and innate immune cells to maintain genomic integrity. However, mutations in BER genes lead to impaired DNA repair function and cause insufficient genomic integrity. Moreover, several studies have implicated that accumulation of DNA damage leads to chromosomal instability that likely activates the innate immune signaling. Furthermore, dysregulation of BER factors in cancer cells modulate the infiltration of innate immune cells to the tumor microenvironment. In the current review, the role of BER in cancer and innate immune cells and its impact on innate immune signaling within the tumor microenvironment is summarized. This is a special issue that focuses on DNA damage and cancer therapy to demonstrate how BER inhibitor or aberrant repair modulates innate inflammatory response and impact immunotherapy approaches. Overall, the review provides substantial evidence to understand the impact of BER in innate immune response dynamics within the current immune-based therapeutic strategy.
Keywords	base excision repair ; innate immune cells ; innate inflammatory signaling ; immunotherapy ; Biology (General) ; QH301-705.5
Subject code	616
Language	English
Publishing date	2022-02-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: A novel role of snail in regulating tuberin/AMPK pathways to promote renal fibrosis in the new mouse model of type II diabetes

Sitai Liang / Mukesh Yadav / Kristine S. Vogel / Samy L. Habib

FASEB BioAdvances, Vol 3, Iss 9, Pp 730-

2021 Volume 743

Abstract: Abstract Epithelial–mesenchymal transition (EMT) plays an important role in tissue fibrosis following chronic exposure to hyperglycemia. This study investigates the role of chronic diabetes in regulating tuberin/snail/AMPK to enhance EMT and increase ... ...

Abstract	Abstract Epithelial–mesenchymal transition (EMT) plays an important role in tissue fibrosis following chronic exposure to hyperglycemia. This study investigates the role of chronic diabetes in regulating tuberin/snail/AMPK to enhance EMT and increase renal fibrosis. A new mouse model of db/db/TSC2+/− was generated by backcrossing db/db mice and TSC2+/− mice. Wild type (WT), db/db, TSC2+/− and dbdb/TSC2+/− mice were sacrificed at ages 6 and 8 months old. Tuberin protein level was significantly decreased in kidneys from diabetic compared to WT mice at both ages. In addition, tuberin and E‐cadherin protein levels were significantly decreased in dbdb/TSC2+/− compared to TSC2+/− and db/db mice. In contrast, p‐PS6K, NFkB, snail, vimentin, fibronectin, and α‐SMA protein levels were significantly increased in dbdb/TSC2+/− compared to db/db and TSC2+/− mice at ages 6 and 8 months. Both downregulation of AMPK by DN‐AMPK and downregulation of tuberin by siRNA resulted in increased NFkB, snail, and fibronectin protein expression and decreased E‐cadherin protein expression in mouse primary renal proximal tubular cells. Interestingly, downregulation of snail by siRNA increased tuberin expression via feedback through activation of AMPK and reversed the expression of epithelial proteins such as E‐cadherin as well as mesenchymal proteins such as fibronectin, NF‐KB, vimentin, and α‐SMA in mouse primary renal proximal tubular cells isolated from kidneys of four mice genotypes. The data show that chronic diabetes significantly decreases tuberin expression and that provides strong evidence that tuberin is a major key protein involved in regulating EMT. These data also demonstrated a novel role for snail in regulating of AMPK/tuberin to enhance EMT and renal cell fibrosis in diabetes.
Keywords	AMPK ; diabetes ; EMT ; fibronectin ; NFkb ; snail ; Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2021-09-01T00:00:00Z
Publisher	Wiley
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Alterations in tubular epithelial cells in diabetic nephropathy.

Habib, Samy L

Journal of nephrology

2013 Volume 26, Issue 5, Page(s) 865–869

Abstract: Renal hypertrophy, matrix protein accumulation and tubulointerstitial fibrosis are major pathological features of diabetic nephropathy (DN) that eventuate in renal failure. Hyperglycemia and high concentration of glucose increase matrix protein ... ...

Abstract	Renal hypertrophy, matrix protein accumulation and tubulointerstitial fibrosis are major pathological features of diabetic nephropathy (DN) that eventuate in renal failure. Hyperglycemia and high concentration of glucose increase matrix protein expression, but the pathogenic mechanisms are not fully understood. We have previously reported that inactivation of tuberin resulting in activation of the mammalian target of rapamycin (mTOR) pathway and increased matrix protein accumulation in cultured proximal tubular cells exposed to high glucose and in kidney cortex of rats with type 1 diabetes. In this report, we show that kidney sections of diabetic patients express higher levels of phospho-tuberin (inactive form of tuberin), and that is associated with an increase in mTOR activation as measured by phosphorylation level of p70S6K. Inactivation of tuberin and activation of mTOR lead to accumulated cell matrix proteins (fibronectin and collagen IV) mainly in tubular epithelial cells of the kidneys of diabetic patients. In addition, significant staining of vimentin as a marker of cells undergoing an epithelial-to-mesenchymal transition (EMT) was detected in kidney sections of diabetic patients. On the other hand, very weak or nondetectable staining of cell matrix proteins, p-tuberin and P-p70S6K as well as vimentin was found in normal kidney sections of healthy subjects. The morphological changes in kidney sections of diabetic patients showed tubular thickening, glomerular and tubular hypertrophy, compared to normal structure of tubuli and glomeruli in kidney from healthy control subjects. These data suggest that alterations in tubular cells' structure, including tubular thickening and hypertrophy, are major mediators of the fibrotic process in DN.
MeSH term(s)	Biomarkers ; Collagen Type IV/metabolism ; Diabetic Nephropathies/metabolism ; Diabetic Nephropathies/pathology ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Epithelial-Mesenchymal Transition ; Fibronectins/metabolism ; Fibrosis ; Humans ; Kidney/metabolism ; Kidney Tubules, Proximal/metabolism ; Kidney Tubules, Proximal/pathology ; Male ; Phosphorylation ; Ribosomal Protein S6 Kinases, 70-kDa/metabolism ; TOR Serine-Threonine Kinases/metabolism ; Tumor Suppressor Proteins/metabolism ; Vimentin/metabolism
Chemical Substances	Biomarkers ; Collagen Type IV ; Fibronectins ; Tumor Suppressor Proteins ; Vimentin ; tuberous sclerosis complex 2 protein (4JG2LF96VF) ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Ribosomal Protein S6 Kinases, 70-kDa (EC 2.7.11.1)
Language	English
Publishing date	2013-09
Publishing country	Italy
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1093991-x
ISSN	1724-6059 ; 1120-3625 ; 1121-8428
ISSN (online)	1724-6059
ISSN	1120-3625 ; 1121-8428
DOI	10.5301/jn.5000287
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Article ; Online: Mechanism of activation of AMPK and upregulation of OGG1 by rapamycin in cancer cells.

Habib, Samy L

Oncotarget

2011 Volume 2, Issue 12, Page(s) 958–959

MeSH term(s)	AMP-Activated Protein Kinases/metabolism ; Antibiotics, Antineoplastic/pharmacology ; DNA Glycosylases/metabolism ; Humans ; Neoplasms/metabolism ; Sirolimus/pharmacology ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	Antibiotics, Antineoplastic ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; DNA Glycosylases (EC 3.2.2.-) ; oxoguanine glycosylase 1, human (EC 3.2.2.-) ; Sirolimus (W36ZG6FT64)
Language	English
Publishing date	2011-12-23
Publishing country	United States
Document type	Editorial ; Research Support, Non-U.S. Gov't
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.381
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