Peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist inhibits transforming growth factor-beta1 and matrix production in human dermal fibroblasts

Zhang, Guoyou; Cheng, Tao; Zheng, Ming‐Hua; Yi, Chenggang; Pan, Hua; Li, Zhijie; Chen, Xing‐Long; Yu, Qing; Jiang, Liangfu; Feiya, Zhou; Li, Xiaoyang; Yang, Jingquan; Chu, Tinggang; Gao, Weiyang

doi:10.1016/j.bjps.2009.06.032

Cited by 27 publications

(21 citation statements)

References 20 publications

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“…6 The effects of rosiglitazone on the expression of PPAR-γ, P-Smad2/3 in HTFs treated by TGF-β1. Serum starved HTFs for 24 h were incubated with vehicle, 5, 10 μM rosiglitazone for 2 h before TGF-β1 (5 ng/ml) was added to incubate for 24 h. The protein expressions of the PPAR-γ and P-Smad2/3 protein were analyzed using Western blot organ fibroblasts [19][20][21]. This result also showed us that HTFs could be treated as a therapeutic target by PPAR-γ agonists.…”

Section: Discussionmentioning

confidence: 97%

Rosiglitazone attenuates activation of human Tenon’s fibroblasts induced by transforming growth factor -β1

Fan

Li²,

Duan

et al. 2012

Graefes Arch Clin Exp Ophthalmol

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Section: Discussionmentioning

confidence: 97%

Rosiglitazone attenuates activation of human Tenon’s fibroblasts induced by transforming growth factor -β1

Fan

Li²,

Duan

et al. 2012

Graefes Arch Clin Exp Ophthalmol

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“…PPAR-␥ ligands have been shown to inhibit Akt/mTOR/S6K activity, TGF-␤ activity, fibrosis, and matrix production in fibroblasts and heart tissue and to decrease ERK activity in endothelial cells (4,12,16,54). The activation of PPAR-␥ can inhibit several components of the cell cycle (43) and has an anti-proliferative effect on epithelial cancer cells (1, 6, 38).…”

Section: Discussionmentioning

confidence: 98%

PPAR-γ agonist ameliorates kidney and liver disease in an orthologous rat model of human autosomal recessive polycystic kidney disease

Yoshihara

Kurahashi²,

Morita

et al. 2011

American Journal of Physiology-Renal Physiology

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In autosomal recessive polycystic kidney disease (ARPKD), progressive enlargement of fluid-filled cysts is due to aberrant proliferation of tubule epithelial cells and transepithelial fluid secretion leading to extensive nephron loss and interstitial fibrosis. Congenital hepatic fibrosis associated with biliary cysts/dilatations is the most common extrarenal manifestation in ARPKD and can lead to massive liver enlargement. Peroxisome proliferator-activated receptor γ (PPAR-γ), a member of the ligand-dependent nuclear receptor superfamily, is expressed in a variety of tissues, including the kidneys and liver, and plays important roles in cell proliferation, fibrosis, and inflammation. In the current study, we determined that pioglitazone (PIO), a PPAR-γ agonist, decreases polycystic kidney and liver disease progression in the polycystic kidney rat, an orthologous model of human ARPKD. Daily treatment with 10 mg/kg PIO for 16 wk decreased kidney weight (% of body weight), renal cystic area, serum urea nitrogen, and the number of Ki67-, pERK1/2-, and pS6-positive cells in the kidney. There was also a decrease in liver weight (% of body weight), liver cystic area, fibrotic index, and the number of Ki67-, pERK1/2-, pERK5-, and TGF-β-positive cells in the liver. Taken together, these data suggest that PIO inhibits the progression of polycystic kidney and liver disease in a model of human ARPKD by inhibiting cell proliferation and fibrosis. These findings suggest that PPAR-γ agonists may have therapeutic value in the treatment of the renal and hepatic manifestations of ARPKD.

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“…PPARG is ubiquitous, with myriad biological effects. It is present in dermal fibroblasts and affects a number of their biological functions [21][22][23]. We therefore hypothesize that the increase in 25-hydroxylation of vitamin D synthesized from the skin in TZD users may be the underlying basis of the higher vitamin D status observed with TZD use.…”

Section: Discussionmentioning

confidence: 96%

Elevated vitamin D status in postmenopausal women on thiazolidinediones for type 2 diabetes

Chakreeyarat

Saetung

Chailurkit

et al. 2010

Endocr

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Thiazolidenediones (TZD) have been reported to lead to non-vertebral bone loss in postmenopausal women with diabetes, but the true incidence of vertebral fractures has been under-detected because two-thirds of vertebral fractures are silent. TZD is also related to increased adiposity, with a consequently greater risk of vitamin D deficiency-both of which seem to aggravate the untoward effect of TZD on bone. The aim of this study is to determine whether TZD use is associated with prevalence of vertebral fractures and low vitamin D status in postmenopausal women with type 2 diabetes. A group of 102 postmenopausal women with type 2 diabetes, 52 TZD users for at least 12 months, and 50 non-TZD users were enrolled in the study. Any data regarding diabetes, age at menopause, co-morbidities, and drug use were recorded. Blood sampling and thoraco-lumbar radiography were performed. Bone mineral density (BMD) of L2-L4 and the femur were measured by dual-energy X-ray absorptiometry (DXA). The occurrence of vertebral fractures at one level or more in subjects on TZD was higher than those not on TZD, but did not reach statistical significance (19.2 vs. 14.0%, P = 0.5). Total hip BMD in subjects on TZD was significantly lower than those not on TZD (0.96 ± 0.15 vs. 1.02 ± 0.11; P < 0.05). Levels of 25(OH)D in TZD users were significantly higher (35.3 ± 1.5 vs. 25.9 ± 1.2 ng/dl; P < 0.001). The prevalence of vitamin D deficiency was 75.5% in subjects not on TZD compared to 34.6% in those on TZD (OR 6.4, 95% CI 2.6-15.6). Higher circulating 25(OH)D was observed in TZD users. TZD use was associated with lower total hip BMD but not with vertebral fracture.

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Peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist inhibits transforming growth factor-beta1 and matrix production in human dermal fibroblasts

Cited by 27 publications

References 20 publications

Rosiglitazone attenuates activation of human Tenon’s fibroblasts induced by transforming growth factor -β1

Rosiglitazone attenuates activation of human Tenon’s fibroblasts induced by transforming growth factor -β1

PPAR-γ agonist ameliorates kidney and liver disease in an orthologous rat model of human autosomal recessive polycystic kidney disease

Elevated vitamin D status in postmenopausal women on thiazolidinediones for type 2 diabetes

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