SREBP contributes to induction of collagen VI transcription by serum starvation

Ferrari, Alessandra; Maretto, Silvia; Girotto, Davide; Volpin, Dino; Bressan, Giorgio M.

doi:10.1016/j.bbrc.2003.11.159

Cited by 12 publications

(9 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is possible (although we cannot demonstrate it in the present study) that the increase in PON1 expression in our patients was related to fibrogenesis. It is known that PON1 and collagen share nuclear transcription factors, such as Sp1 [34,35] and the sterol regulatory elementbinding protein [36,37], and that both genes are linked together in chromosome 7q [38,39]. It is likely, then, that chronic stimulus enhancing collagen expression would also affect PON1 in a similar manner.…”

Section: Discussionmentioning

confidence: 96%

Paraoxonase-1 is associated with oxidative stress, fibrosis and FAS expression in chronic liver diseases

Ferré

Marsillach

Camps

et al. 2006

Journal of Hepatology

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 96%

Paraoxonase-1 is associated with oxidative stress, fibrosis and FAS expression in chronic liver diseases

Ferré

Marsillach

Camps

et al. 2006

Journal of Hepatology

View full text Add to dashboard Cite

“…Transcriptional activation of genes has been identified in cells rendered quiescent by serum starvation (Schneider et al, 1988;Ferrari et al, 2004;Gu et al, 2005;Yabuta et al, 2006). In general, serum starvation induces the cells to enter into the G 0 phase, where they remain in a quiescent state.…”

Section: Discussionmentioning

confidence: 99%

Enhancement of prostaglandin D2 production through cyclooxygenase-2 and lipocalin-type prostaglandin D synthase by upstream stimulatory factor 1 in human brain-derived TE671 cells under serum starvation

Fujimori

Aritake

Urade

2008

Gene

View full text Add to dashboard Cite

“…In addition to its effects on TGF-b synthesis, SREBP-1 may also affect matrix accumulation in alternate ways, such as its regulation of collagen 6a1 transcription in 3T3 cells. 37 Plasminogen activator inhibitor-1, which inhibits matrix breakdown, was also identified as an SREBP-1c transcriptional target in adipocytes. 38 These data suggest that SREBP-1 is an important regulator of organ fibrosis.…”

Section: Discussionmentioning

confidence: 99%

SREBP-1 Mediates Angiotensin II-Induced TGF-β1 Upregulation and Glomerular Fibrosis

Wang

Chen

et al. 2015

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

Angiotensin II is an important mediator of CKD of diverse etiology. A common pathologic feature of CKD is glomerular fibrosis, a central mediator of which is the profibrotic cytokine TGF-b. The mechanisms underlying the induction of TGF-b and matrix by angiotensin II are not completely understood. Recent studies showed that overexpression of the transcription factor SREBP-1 induces glomerular sclerosis and that angiotensin II can activate SREBP-1 in tubular cells. We thus studied whether SREBP-1 is activated by angiotensin II and mediates angiotensin II-induced profibrogenic responses in primary rat mesangial cells. Treatment of cells with angiotensin II induced the upregulation and activation of SREBP-1. Angiotensin II-induced activation of SREBP-1 required signaling through the angiotensin II type I receptor and activation of PI3K/Akt in addition to the chaperone SCAP and protease S1P. Notably, angiotensin II-induced endoplasmic reticulum stress was identified as a key mediator of Akt-SREBP-1 activation, and inhibition of endoplasmic reticulum stress or SREBP-1 prevented angiotensin II-induced SREBP-1 binding to the TGF-b promoter, TGF-b upregulation, and downstream fibronectin upregulation. Endoplasmic reticulum stress alone, however, did not induce TGF-b upregulation despite activating SREBP-1. Although not required for SREBP-1 activation by angiotensin II, EGF receptor signaling was necessary for activation of the SREBP-1 cotranscription factor Sp1, which provided a required second signal for TGF-b upregulation. In vivo, endoplasmic reticulum stress and SREBP-1-dependent effects were induced in glomeruli of angiotensin II-infused mice, and administration of the SREBP inhibitor fatostatin prevented angiotensin II-induced TGF-b upregulation and matrix accumulation. SREBP-1 and endoplasmic reticulum stress thus provide potential novel therapeutic targets for the treatment of CKD.

show abstract

SREBP contributes to induction of collagen VI transcription by serum starvation

Cited by 12 publications

References 17 publications

Paraoxonase-1 is associated with oxidative stress, fibrosis and FAS expression in chronic liver diseases

Paraoxonase-1 is associated with oxidative stress, fibrosis and FAS expression in chronic liver diseases

Enhancement of prostaglandin D2 production through cyclooxygenase-2 and lipocalin-type prostaglandin D synthase by upstream stimulatory factor 1 in human brain-derived TE671 cells under serum starvation

SREBP-1 Mediates Angiotensin II-Induced TGF-β1 Upregulation and Glomerular Fibrosis

Contact Info

Product

Resources

About