Type VIII Collagen Modulates TGF-β1-induced Proliferation of Mesangial Cells

Loeffler, Ivonne; Hopfer, Ulrike; Koczan, Dirk; Wolf, Günter

doi:10.1681/asn.2010010098

Cited by 46 publications

(34 citation statements)

References 58 publications

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“…Rather, it can regulate tissue remodeling by mediating fibrotic signaling and processes in smooth muscle cells. [230][231][232] Thus, we speculated that collagen VIII could regulate the integrity of the LV indirectly by promoting fibrotic remodeling by cardiac fibroblasts. In line with this, we showed attenuated TGF-β1 signaling, reduced production of structural collagens I and III and decreased myofibroblast differentiation after pressure overload in mice lacking collagen VIII.…”

Section: The Multiple Roles Of Syndecan-4 In Cardiac Remodelingmentioning

confidence: 99%

Innate immune signaling induces expression and shedding of the heparan sulfate proteoglycan syndecan‐4 in cardiac fibroblasts and myocytes, affecting inflammation in the pressure‐overloaded heart

et al. 2013

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Sustained pressure overload induces heart failure, the main cause of mortality in the Western world. Increased understanding of the underlying molecular mechanisms is essential to improve heart failure treatment. Despite important functions in other tissues, cardiac proteoglycans have received little attention. Syndecan‐4, a transmembrane heparan sulfate proteoglycan, is essential for pathological remodeling, and we here investigated its expression and shedding during heart failure. Pressure overload induced by aortic banding for 24 h and 1 week in mice increased syndecan‐4 mRNA, which correlated with mRNA of inflammatory cytokines. In cardiac myocytes and fibroblasts, tumor necrosis factor‐α, interleukin‐1β and lipopolysaccharide through the toll‐like receptor‐4, induced syndecan‐4 mRNA. Bioinformatical and mutational analyses in HEK293 cells identified a functional site for the proinflammatory nuclear factor‐κB transcription factor in the syndecan‐4 promoter, and nuclear factor‐κB regulated syndecan‐4 mRNA in cardiac cells. Interestingly, tumor necrosis factor‐α, interleukin‐1β and lipopolysaccharide induced nuclear factor‐κB‐dependent shedding of the syndecan‐4 ectodomain from cardiac cells. Overexpression of syndecan‐4 with mutated enzyme‐interacting domains suggested enzyme‐dependent heparan sulfate chains to regulate shedding. In cardiac fibroblasts, lipopolysaccharide reduced focal adhesion assembly, shown by immunohistochemistry, suggesting that inflammation‐induced shedding affects function. After aortic banding, a time‐dependent cardiac recruitment of T lymphocytes was observed by measuring CD3, CD4 and CD8 mRNA, which was reduced in syndecan‐4 knockout hearts. Finally, syndecan‐4 mRNA and shedding were upregulated in failing human hearts. Conclusively, our data suggest that syndecan‐4 plays an important role in the immune response of the heart to increased pressure, influencing cardiac remodeling and failure progression.

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Section: The Multiple Roles Of Syndecan-4 In Cardiac Remodelingmentioning

confidence: 99%

Innate immune signaling induces expression and shedding of the heparan sulfate proteoglycan syndecan‐4 in cardiac fibroblasts and myocytes, affecting inflammation in the pressure‐overloaded heart

et al. 2013

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“…Interestingly, FGF21 and its receptor components are expressed locally in the kidney and increased significantly in both mesangial and tubular cells in diabetic mouse [34,35]. Therefore, FGF21 may have direct actions in kidney injury and repair in diabetic nephropathy.…”

mentioning

confidence: 99%

The role of fibroblast growth factor 21 in diabetes and its complications: A review from clinical perspective

Liu

Foo

Liu

et al. 2015

Diabetes Research and Clinical Practice

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“…In diabetic nephropathy, mesangial cell proliferation has been proposed to play a role in the progression of glomerulosclerosis [38][39].…”

Section: The Role Of Connexins In the Diabetic Kidneymentioning

confidence: 99%

Mind the gap: connexins and cell–cell communication in the diabetic kidney

2014

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Connexins, assembled as a hexameric connexon, form a transmembrane hemichannel that provides a conduit for paracrine signalling of small molecules and ions to regulate the activity and function of adjacent cells. When hemichannels align and associate with similar channels on opposing cells, they form a continuous aqueous pore or gap junction, allowing the direct transmission of metabolic and electrical signals between coupled cells. Regulation of gap junction synthesis and channel activity is critical for cell function, and a number of diseases can be attributed to changes in the expression/function of these important proteins. Diabetic nephropathy is associated with several complex metabolic and inflammatory responses characterised by defects at the molecular, cellular and tissue level. In both type 1 and type 2 diabetes, glycaemic injury of the kidney is the leading cause of end-stage renal failure, a consequence of multiple aetiologies, including increased deposition of extracellular matrix, glomerular hyperfiltration, albuminuria and tubulointerstitial fibrosis. In diabetic nephropathy, loss of connexin mediated cell-cell communication within the nephron may represent an early sign of disease; however, our current knowledge of the role of connexins in the diabetic kidney is sparse. This review highlights recent evidence demonstrating that maintained connexin-mediated cell-cell communication could benefit region-specific renal function in diabetic nephropathy and suggests that these proteins should be viewed as a tantalising novel target for therapeutic intervention.

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Type VIII Collagen Modulates TGF-β1-induced Proliferation of Mesangial Cells

Cited by 46 publications

References 58 publications

Innate immune signaling induces expression and shedding of the heparan sulfate proteoglycan syndecan‐4 in cardiac fibroblasts and myocytes, affecting inflammation in the pressure‐overloaded heart

Innate immune signaling induces expression and shedding of the heparan sulfate proteoglycan syndecan‐4 in cardiac fibroblasts and myocytes, affecting inflammation in the pressure‐overloaded heart

The role of fibroblast growth factor 21 in diabetes and its complications: A review from clinical perspective

Mind the gap: connexins and cell–cell communication in the diabetic kidney

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