Vitamin D: a novel therapeutic approach for keloid, an in vitro analysis

Zhang, G.Y.; Cheng, Tao; Luan, Qi; Liao, Tian; Nie, Chunlei; Zheng, Xin; Xie, Xue-guan; Gao, Weiyang

doi:10.1111/j.1365-2133.2010.10130.x

Cited by 62 publications

(50 citation statements)

References 34 publications

(54 reference statements)

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“…The most commonly used modalities are pressure, silicone gel sheet, intralesional steroids, 5-fluorouracil (5 FU), cryotherapy, surgical excision, and lasers [12]. Furthermore, photodynamic therapy [24] and topical application of vitamin D [33] were also reported as novel therapeutic approaches for keloid nodules. Pirfenidone is expected to be another remedy in the arsenal against keloid lesions in the form of either oral or topical administration.…”

Section: Discussionmentioning

confidence: 99%

Pirfenidone suppresses keloid fibroblast-embedded collagen gel contraction

et al. 2011

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Keloid is a clinically intractable disease that causes disfigurement, itching, and pain due to abnormal proliferation of fibroblasts and production of collagen. Pirfenidone is a novel anti-fibrotic agent that inhibits the progression of fibrosis occurring in the keloid lesions of the lung and kidney. In order to examine whether pirfenidone has a therapeutic effect on keloid lesions, we prepared an in vitro wound contraction model with keloid fibroblasts. The gel contractility of a mixture of keloid fibroblasts and an acid-soluble collagen solution was examined with/without transforming growth factor (TGF)-β1 in the presence or absence of pirfenidone. Real time RT-PCR was performed to detect mRNA expression of TGFB1, CTGF, aSMA, and Col1A1 quantitatively in keloid fibroblasts incubated with/without TGF-β1 in the presence or absence of pirfenidone. The contractility of keloid fibroblast-embedded collagen gel was increased after the addition of TGF-β1. Pirfenidone suppressed gel contraction with TGF-β1 dose dependently. TGF-β1 stimulated mRNA expression of TGFB1, CTGF, aSMA, and Col1A1 in keloid fibroblasts, while pirfenidone significantly inhibited mRNA expression of CTGF and aSMA in the identical cells. These findings suggest that pirfenidone suppresses the contraction of keloid-derived fibroblasts by inhibiting the down-stream pathway of TGF-β1, thus demonstrating its therapeutic utility for the treatment of keloid lesions.

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Section: Discussionmentioning

confidence: 99%

Pirfenidone suppresses keloid fibroblast-embedded collagen gel contraction

et al. 2011

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“…Recent studies also suggest a beneficial role of vitamin D in slowing the progression of tissue fibrosis. A previous study in vivo revealed vitamin D supplements increase promoter activity of cultured keloid fibroblasts and decrease fibrosis, suggesting that vitamin D supplementation could be a preventive early treatment strategy for keloid and related fibrotic disorders [8]. …”

Section: Introductionmentioning

confidence: 99%

“…The expression of VDR in cultured keloid fibroblasts has been confirmed [8]; however, there is no study regarding the association between VDR level and KS in a clinical setting. In addition, whether the genetic variants of VDR are associated with the risk for KS has not been investigated In this study, we enrolled KS patients and healthy controls to testify this possible association.…”

Section: Introductionmentioning

confidence: 99%

The TaqI Gene Polymorphisms of VDR and the Circulating 1,25-Dihydroxyvitamin D Levels Confer the Risk for the Keloid Scarring in Chinese Cohorts

Shang

Luo

et al. 2013

Cell Physiol Biochem

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Aim: to investigate the association between vitamin D receptor polymorphisms and circulating 1,25-Dihydroxyvitamin D (1,25(OH)2D) levels with keloid scar (KS) risk. Methods: A total of 261 patients with KS and 261 normal healthy individuals were enrolled. VDR gene polymorphisms were determined. Circulating 1,25(OH)2D levels were detected. Results: In this study, we investigated the role of four loci of VDR gene polymorphisms in determining the risk of KS in a Chinese cohort. We found that the TaqI C>T polymorphism was closely associated with the KS incidence. Carriers with CC genotype of TaqI had a higher chance of developing KS. Stratification analyses by sex showed that this trend exists only in female subjects but not in male subjects. Furthermore, the TaqI C>T polymorphism affects the circulating 25-Hydroxyvitamin D levels. The CC carriers had a significantly lower mean circulating 1,25(OH)2D level than TT carriers and CT carriers. KS subjects had significantly lower mean serum circulating 1,25(OH)2D level than controls. The receiver operating characteristic curve analysis revealed that the serum circulating 1,25(OH)2D level at the cut-off point of 16.1 ng/ml could discriminate KS subjects from controls. Conclusion: Collectively, these data provide evidence that the vitamin D/VDR pathway plays an important role in the development of KS. The TaqI gene polymorphisms of VDR and circulating 1,25(OH)2D levels may thus be used as potential markers for prediction of KS development.

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“…For example, a Rac1 inhibitor [5], IFN-g [6], a p38 inhibitor [7], Vitamin D [8], SB431542 (TGF-b1 inhibitor) [9], a PPAR-g agonist [10] and CTGF antisense oligonucleotides [11] can inhibit the increase in collagen and a-SMA expression induced by TGF-b. PPAR-g activation and CTGF inhibition were also effective in in vivo models of fibrosis [12,13].…”

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confidence: 99%