Genistein Attenuates Advanced Glycation End Product-Induced Expression of Fibronectin and Connective Tissue Growth Factor

Tong, Mengli; Wang, Yuhui; Wang, Yongjun; Chen, Hongyu; Cheng-da, Wang; Yang, Luchun; Axelsson, Jonas; Lindholm, Bengt

doi:10.1159/000339168

Cited by 7 publications

(3 citation statements)

References 85 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This promotes mesothelial cell production of fibronectin via the induction of the ERK1/2 and MAPK pathways thereby contributing to peritoneal injury and inflammation ( Kiribayashi et al, 2005 ). The increased production of fibronectin by mesothelial cells can also be induced by the presence of advanced glycation end products (AGEs; Tong et al, 2012 ).…”

Section: Mesothelial Cell Functionsmentioning

confidence: 99%

“…Other cell sources that may be used for mesothelial repair include bone marrow derived cells ( Sekiguchi et al, 2012 ), adipose-derived stem cells ( Kim et al, 2014 ), and mesenchymal stem cells ( Wang et al, 2012 ; Ueno et al, 2013 ). Alternative therapeutic strategies being investigated to reduce mesothelial cell-mediated inflammation and prevent peritoneal fibrosis include targeting TGFβ1-mediated mechanisms ( Hung et al, 2001 , 2003 ; Yung et al, 2001 ; Margetts et al, 2002a ; Fang et al, 2006 ; Tomino, 2012 ; Jang et al, 2013 ), reducing mesothelial cell production of fibronectin ( Tong et al, 2012 ; Zhang et al, 2014 ) developing a more bio compatible PD solution ( Bajo et al, 2000 ; Le Poole et al, 2005 ), altering PD daily dwelling time ( Lee et al, 2014 ), and stimulating fibrinolytic agents ( Haslinger et al, 2003 ).…”

Section: The Mesothelial Cell In Fibrotic Disordersmentioning

confidence: 99%

See 1 more Smart Citation

Mesothelial cells in tissue repair and fibrosis

et al. 2015

View full text Add to dashboard Cite

Mesothelial cells are fundamental to the maintenance of serosal integrity and homeostasis and play a critical role in normal serosal repair following injury. However, when normal repair mechanisms breakdown, mesothelial cells take on a profibrotic role, secreting inflammatory, and profibrotic mediators, differentiating and migrating into the injured tissues where they contribute to fibrogenesis. The development of new molecular and cell tracking techniques has made it possible to examine the origin of fibrotic cells within damaged tissues and to elucidate the roles they play in inflammation and fibrosis. In addition to secreting proinflammatory mediators and contributing to both coagulation and fibrinolysis, mesothelial cells undergo mesothelial-to-mesenchymal transition, a process analogous to epithelial-to-mesenchymal transition, and become fibrogenic cells. Fibrogenic mesothelial cells have now been identified in tissues where they have not previously been thought to occur, such as within the parenchyma of the fibrotic lung. These findings show a direct role for mesothelial cells in fibrogenesis and open therapeutic strategies to prevent or reverse the fibrotic process.

show abstract

Section: Mesothelial Cell Functionsmentioning

confidence: 99%

Section: The Mesothelial Cell In Fibrotic Disordersmentioning

confidence: 99%

Mesothelial cells in tissue repair and fibrosis

et al. 2015

View full text Add to dashboard Cite

show abstract

“…The production level of ECM is increased by IL-1β, TNF-α, EGF, and TGF-β [65][66][67][68][69][70][71][72][73][74][75]. The renin-angiotensin system or AGEs also stimulates ECM production [76,77]. MC provides a protective and non-adhesive surface for intracoelomic organs and tissues.…”

Section: Synthesis Of Extracellular Matrix (Ecm)mentioning

confidence: 99%

Diverse properties of the mesothelial cells in health and disease

Kawanishi¹

2016

Pleura and Peritoneum

View full text Add to dashboard Cite

Mesothelial cells (MCs) form the superficial anatomic layer of serosal membranes, including pleura, pericardium, peritoneum, and the tunica of the reproductive organs. MCs produce a protective, non-adhesive barrier against physical and biochemical damages. MCs express a wide range of phenotypic markers, including vimentin and cytokeratins. MCs play key roles in fluid transport and inflammation, as reflected by the modulation of biochemical markers such as transporters, adhesion molecules, cytokines, growth factors, reactive oxygen species and their scavengers. MCs synthesize extracellular matrix related molecules, and the surface of MC microvilli secretes a highly hydrophilic protective barrier, “glycocalyx”, consisting mainly of glycosaminoglycans. MCs maintain a balance between procoagulant and fibrinolytic activation by producing a whole range of regulators, can synthetize fibrin and therefore form adhesions. Synthesis and recognition of hyaluronan and sialic acids might be a new insight to explain immunoactive and immunoregulatory properties of MCs. Epithelial to mesenchymal transition of MCs may involve serosal repair and remodeling. MCs might also play a role in the development and remodeling of visceral adipose tissue. Taken together, MCs play important roles in health and disease in serosal cavities of the body. The mesothelium is not just a membrane and should be considered as an organ.

show abstract

Assessment of early renal damage in diabetic rhesus monkeys

Wang

Liu

et al. 2014

Endocrine

View full text Add to dashboard Cite

The objectives of the study were to improve the model system of diabetic nephropathy in nonhuman primates and assess the early renal damage. Diabetes was induced in monkeys by streptozotocin, and the animals were administered exogenous insulin to control blood glucose (BG). Animals were divided into four groups, including the normal group (N = 3), group A (streptozotocin diabetic model with control of BG < 10 mmol/L, N = 3), group B (streptozotocin diabetic model with control of BG between 15 and 20 mmol/L, N = 4), and group C (streptozotocin diabetic model with control of BG between 15 and 20 mmol/L and high-sodium and high-fat diet, N = 4). The following parameters were evaluated: (1) blood biochemistry and routine urinalysis, (2) color Doppler ultrasound, (3) angiography, (4) renal biopsy, and (5) renal fibrosis-related gene expression levels. Animals in group C developed progressive histologic changes with typical diabetic nephropathy resembling diabetic nephropathy in human patients and exhibited accelerated development of diabetic nephropathy compared with other nonhuman primate models. Significant changes in the expression of the Smad2/3 gene and eNOS in renal tissue were also observed in the early stage of diabetic nephropathy. In conclusion, our model is an excellent model of diabetic nephropathy for understanding the pathogenesis of diabetic nephropathy.

show abstract

Genistein Attenuates Advanced Glycation End Product-Induced Expression of Fibronectin and Connective Tissue Growth Factor

Cited by 7 publications

References 85 publications

Mesothelial cells in tissue repair and fibrosis

Mesothelial cells in tissue repair and fibrosis

Diverse properties of the mesothelial cells in health and disease

Assessment of early renal damage in diabetic rhesus monkeys

Contact Info

Product

Resources

About