Streptozocin Diabetes Elevates all Isoforms of TGF-β in the Rat Kidney

Transforming growth factor beta (TGF-β) is a major promoter of diabetic nephropathy. While TGF-β1 is the most abundaft renal isoform, types 2 and 3 are present as well and have identicalin vitroeffects. Whole kidney extracts were studied 2 weeks after induction of streptozocin diabetes and in control rats. Mean glomerular area was 25% greater in the diabetic animals. TGF-β1 showed a 2-fold increase in message with a 3-fold increase in protein. TGF-β2 mRNA increased approximately 6% while its protein doubled. TGF-β-message increased by 25%, producing a 35% increase in its protein. TGF-β- inducible gene H3 mRNA was increased 35% in the diabetic animals, consistent with increased activity of this growth factor. All isoforms of TGF-β are increased in the diabetic rat kidney. Future studies need to address the specific role that each isoform plays in diabetic nephropathy as well as the impact of therapies on each isoform.

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Effects of transforming growth factor-beta 1 (TGF-β1) on in vitro mineralization of human osteoblasts on implant materials

Biomaterials ◽

10.1016/s0142-9612(02)00616-6 ◽

2003 ◽

Vol 24 (12) ◽

pp. 2013-2020 ◽

Cited By ~ 68

Author(s):

Hai Zhang ◽

Mansur Ahmad ◽

Gloria Gronowicz

Keyword(s):

Growth Factor ◽

Transforming Growth Factor Beta ◽

Transforming Growth Factor ◽

Human Osteoblasts ◽

Implant Materials ◽

In Vitro Mineralization ◽

Growth Factor Beta ◽

Tgf Β1

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DPSCs treated by TGF-β1 regulate angiogenic sprouting of three-dimensionally co-cultured HUVECs and DPSCs through VEGF-Ang-Tie2 signaling

Stem Cell Research & Therapy ◽

10.1186/s13287-021-02349-y ◽

2021 ◽

Vol 12 (1) ◽

Author(s):

Yuchen Zhang ◽

Junqing Liu ◽

Ting Zou ◽

Yubingqing Qi ◽

Baicheng Yi ◽

...

Keyword(s):

Stem Cells ◽

Growth Factor ◽

Blood Vessels ◽

Western Blotting ◽

Transforming Growth Factor Beta ◽

Transforming Growth Factor ◽

Vegf Receptor ◽

Vegfr2 Signaling ◽

Tgf Β1

Abstract Background Maintaining the stability and maturation of blood vessels is of paramount importance for the vessels to carry out their physiological function. Smooth muscle cells (SMCs), pericytes, and mesenchymal stem cells (MSCs) are involved in the maturation process of the newly formed vessels. The aim of this study was to investigate whether transforming growth factor beta 1 (TGF-β1) treatment could enhance pericyte-like properties of dental pulp stem cells (DPSCs) and how TGF-β1-treated DPSCs for 7 days (T-DPSCs) stabilize the newly formed blood vessels. Methods We utilized TGF-β1 to treat DPSCs for 1, 3, 5, and 7 days. Western blotting and immunofluorescence were used to analyze the expression of SMC markers. Functional contraction assay was conducted to assess the contractility of T-DPSCs. The effects of T-DPSC-conditioned media (T-DPSC-CM) on human umbilical vein endothelial cell (HUVEC) proliferation and migration were examined by MTT, wound healing, and trans-well migration assay. Most importantly, in vitro 3D co-culture spheroidal sprouting assay was used to investigate the regulating role of vascular endothelial growth factor (VEGF)-angiopoietin (Ang)-Tie2 signaling on angiogenic sprouting in 3D co-cultured spheroids of HUVECs and T-DPSCs. Angiopoietin 2 (Ang2) and VEGF were used to treat the co-cultured spheroids to explore their roles in angiogenic sprouting. Inhibitors for Tie2 and VEGFR2 were used to block Ang1/Tie2 and VFGF/VEGFR2 signaling. Results Western blotting and immunofluorescence showed that the expression of SMC-specific markers (α-SMA and SM22α) were significantly increased after treatment with TGF-β1. Contractility of T-DPSCs was greater compared with that of DPSCs. T-DPSC-CM inhibited HUVEC migration. In vitro sprouting assay demonstrated that T-DPSCs enclosed HUVECs, resembling pericyte-like cells. Compared to co-culture with DPSCs, a smaller number of HUVEC sprouting was observed when co-cultured with T-DPSCs. VEGF and Ang2 co-stimulation significantly enhanced sprouting in HUVEC and T-DPSC co-culture spheroids, whereas VEGF or Ang2 alone exerted insignificant effects on HUVEC sprouting. Blocking Tie2 signaling reversed the sprouting inhibition by T-DPSCs, while blocking VEGF receptor (VEGFR) signaling boosted the sprouting inhibition by T-DPSCs. Conclusions This study revealed that TGF-β1 can induce DPSC differentiation into functional pericyte-like cells. T-DPSCs maintain vessel stability through Ang1/Tie2 and VEGF/VEGFR2 signaling.

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HUBUNGAN ANTARA KADAR TGF-Β1 DENGAN KADAR ALBUMIN DALAM URIN PASIEN DM TIPE-2 DENGAN NEFROPATI DIABETIK

JAMBI MEDICAL JOURNAL Jurnal Kedokteran dan Kesehatan ◽

10.22437/jmj.v7i1.7070 ◽

2019 ◽

Vol 7 (1) ◽

pp. 73-81

Author(s):

Elfiani Elfiani ◽

Rita Halim ◽

M Haldian Hakir

Keyword(s):

Diabetic Nephropathy ◽

Growth Factor ◽

Transforming Growth Factor Beta ◽

Transforming Growth Factor ◽

Transforming Growth Factor Β1 ◽

Albumin Level ◽

Cross Sectional ◽

Integrin Linked Kinase ◽

Tgf Β1

ABSTRACT Background: Diabetic nephropathy (DN) is a complication of diabetes in the kidney that frequently causes terminal kidney disease. This kidney disease caused by diabetes is a syndrome characterized by albumin in urine (albuminuria). Growth factor-β1 (TGF- β1) is a multifunctional cytokine that controls many biological processes, including immunity, differentiation, tumor suppression, tumor metastasis, aging, migration, wound healing, apoptosis, adipogenesis, and osteogenesis. Previous studies had showed that TGF-β1 plays a role in albuminuria, where TGF-β1 expression in the kidney increases in diabetes patients. Elevation of cytokine level, especially transforming growth factor beta-1 (TGF-β1) that induces the increase of several extra cellular matrices (ECM), i.e. fibronectin, integrin-linked kinase (ILK) and type IV collagen. This TGF-β1 activity causes the accumulation of ECM, which leads to thickened glomerular basement membrane (GBM). Thickening of GBM and changes in kidney structure in the form of hypertrophy and reduced glomerular podocytes caused by apoptosis and attachment in GBM causes protein components to exit through urine (albuminuria). This study aimed to prove the correlation between transforming growth factor-β1 and albumin level in urine of diabetic nephropathy. Metode : This study a observasional with desain Cross-sectional comparative study. Results: Mean TGF-β1 level in type 2 DM patients with diabetic nephropathy in this study was 47.30 ± 14.70 ng/ml, with similar value between men and women with 43.1 ng/ml and 44.7 ng/ml, respectively. Out of 60 type 2 DM participants with ND, the mean albuminuria level according to ACR was 722.53 ± 1854.96 mg/g. The result of male participants was lower compared to female participants, with 667.8 mg/mg and 777.2 mg/g, respectively. Conclusion: There was insignificant correlation between TGF-β1 in diabetic nephropathy (DN) and albumin level in urine measured using albumin and urine creatinine ratio (ACR) (p = 0.066). Keywords: Diabetic Nephropathy, Albuminuria, TGF-β1 ABSTRAK Latar Belakang : Nefropati diabetik (ND) merupakan komplikasi diabetes pada ginjal yang paling sering menyebabkan terjadinya penyakit ginjal terminal. Penyakit ginjal akibat diabetes ini merupakan sindroma dengan karakteristik terdapatnya albumin dalam urine (albuminuria). Faktor pertumbuhan-β1 (TGF-β1) adalah sebuah sitokin multifungsi yang mengendalikan banyak proses biologis termasuk kekebalan, diferensiasi, tumor supresi, tumor metastasis, penuaan, migrasi, penyembuhan luka, apoptosis, adipogenesis, dan osteogenesis. Sejumlah penelitian sebelumnya menunjukkan bahwa TGF-β1 berperan terhadap terjadinya albuminuria, dimana pasien diabetes didapatkan ekspresi TGF-β1 di ginjal meningkat. Peningkatan kadar cytokine terutama Transforming Growth Factor Beta-1 (TGF-β1) yang menginduksi peningkatan beberapa Extra Cellular Matrix (ECM) antara lain fibronectin, integrin-linked kinase (ILK) dan collagen tipe-IV. Aktifitas TGF-β1 ini menyebabkan akumulasi ECM sehingga terjadi penebalan Glomerular Basement Membrane (GBM). Penebalan dari GBM dan terjadinya perubahan struktur ginjal berupa hipertrofi dan berkurangnya sel-sel podocyte glomerulus akibat kerusakan (apoptosis) dan perlengketan di GBM menyebabkan komponen protein keluar melalui urin (albuminuria). Tujuan penelitian ini untuk membuktikan hubungan antara kadar transforming growth factor-β1 dengan kadar albumin dalam urin pada Nefropati Diabetik. Metode : Penelitian ini merupakan penelitian Observasional dengan desain Cross-sectional comparative study. Hasil : Kadar rata-rata TGF-β1 pasien DM tipe-2 dengan Nefropati Diabetik pada penelitian ini adalah 47,30 ± 14,70 ng/ml, tidak jauh berbeda antara laki-laki yaitu 43,1 ng/ml dengan perempuan 44,7 ng/ml. Dari 60 orang responden DM tipe-2 dengan ND pada penelitian ini didapatkan kadar albuminuria rata-rata berdasarkan ACR adalah 722,53 ± 1854,96 mg/g. Responden laki-laki lebih rendah dibanding perempuan yaitu 667,8 mg/g berbanding 777,2 mg/g. Kesimpulan : Tidak terdapat hubungan yang bermakna antara TGF-β1 pada Nefropati Diabetik (ND) dengan kadar albumin dalam urin yang dihitung berdasarkan rasio albumin dan creatinin urin (ACR) (p=0,066). Kata Kunci : Nefropati Diabetik, Albuminuria, TGF-β1

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A phorbol ester-regulated ribonuclease system controlling transforming growth factor beta 1 gene expression in hematopoietic cells

Molecular and Cellular Biology ◽

10.1128/mcb.10.11.5983-5990.1990 ◽

1990 ◽

Vol 10 (11) ◽

pp. 5983-5990

Author(s):

R E Wager ◽

R K Assoian

Keyword(s):

Gene Expression ◽

Growth Factor ◽

Transforming Growth Factor Beta ◽

Transforming Growth Factor ◽

Fold Increase ◽

Mrna Levels ◽

Tgf Beta ◽

Growth Factor Beta

12-Tetradecanoylphorbol-13-acetate (TPA)-induced differentiation of U937 promonocytes leads to a 30-fold increase in transforming growth factor beta 1 (TGF-beta 1) gene expression, and this effect results from a stabilized mRNA. Similar up-regulation was detected in TPA-treated K562 erythroblasts but was absent from cell lines that do not differentiate in response to TPA. Related studies in vitro showed that postnuclear extracts of U937 promonocytes contain a ribonuclease system that degrades TGF-beta 1 mRNA selectively and that this system is completely blocked by prior treatment of the cells with TPA. These data identify a new mechanism for regulating TGF-beta 1 mRNA levels and allow us to establish the overall basis for control of TGF-beta 1 gene expression by activation of protein kinase C. Our results also provide a new basis for understanding the long-term up-regulation of TGF-beta 1 gene expression that can accompany hematopoietic cell differentiation.

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Transforming growth factor-beta2 antibody attenuates fibrosis in the experimental diabetic rat kidney

Journal of Endocrinology ◽

10.1677/joe.0.1700647 ◽

2001 ◽

Vol 170 (3) ◽

pp. 647-651 ◽

Cited By ~ 58

Author(s):

C Hill ◽

A Flyvbjerg ◽

R Rasch ◽

M Bak ◽

A Logan

Keyword(s):

Diabetic Nephropathy ◽

Growth Factor ◽

Western Blotting ◽

Transforming Growth Factor ◽

Rat Kidney ◽

Human Monoclonal Antibody ◽

Diabetic Rats ◽

Diabetic Rat ◽

Diabetic Kidney ◽

In The Diabetic Kidney

Diabetic nephropathy is characterised by an increase in glomerular and tubular fibrosis that compromises kidney function. The transforming growth factor-betas (TGF-betas) have been shown to play a major role in fibrosis and we have shown that TGF-beta2, in particular, increases co-ordinately with fibrogenesis in the diabetic kidney. The aim of this study was to investigate the changes in expression of extracellular matrix molecules in the diabetic kidney, with and without systemic administration of a recombinant human monoclonal antibody to TGF-beta2. Streptozotocin-induced diabetic rats were split into two groups. The first were treated with 5 mg/kg irrelevant control IgG4 (placebo) and the second treated with 5 mg/kg isoform-specific recombinant monoclonal anti-TGF-beta2 IgG4 (termed CAT-152) systemically every second day for 14 days. A further group of six non-diabetic rats was also used as a control. Various biological parameters were measured daily throughout the experimental period, and on termination of the experiment at 14 days Western blotting was performed on kidney cortices for procollagen-I C-propeptide, which is an indicator of the rate of collagen-I synthesis within the kidney. In the placebo-treated diabetic rats, blood glucose, food consumption, urinary albumin excretion (UAE) and kidney weights were all significantly higher than in the non-diabetic group (P<0.05, n=24, by ANOVA). In the anti-TGF-beta2-treated diabetic rats, kidney weights and UAE levels were decreased when compared with those in placebo-treated diabetics. Western blotting for the procollagen-I C-propeptide in kidney cortices showed a significant increase in levels in placebo-treated diabetic rats compared with non-diabetic controls over the 14 day diabetic period, indicating initiation of fibrogenesis. By contrast, in anti-TGF-beta2-treated diabetic rats, levels of the propeptide remained at non-diabetic levels. In summary, a significant suppression of kidney fibrosis was seen in anti-TGF-beta2-treated diabetic rats, compared with placebo-treated diabetic rats. We conclude that systemic delivery of CAT-152, a neutralising anti-TGF-beta2 antibody, during the acute stages of diabetic nephropathy reduces the rate of pathogenic fibrosis in the kidney.

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A phorbol ester-regulated ribonuclease system controlling transforming growth factor beta 1 gene expression in hematopoietic cells.

Molecular and Cellular Biology ◽

10.1128/mcb.10.11.5983 ◽

1990 ◽

Vol 10 (11) ◽

pp. 5983-5990 ◽

Cited By ~ 30

Author(s):

R E Wager ◽

R K Assoian

Keyword(s):

Gene Expression ◽

Growth Factor ◽

Transforming Growth Factor Beta ◽

Transforming Growth Factor ◽

Fold Increase ◽

Mrna Levels ◽

Tgf Beta ◽

Growth Factor Beta

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Tethered TGF-β1 in a Hyaluronic Acid-Based Bioink for Bioprinting Cartilaginous Tissues

International Journal of Molecular Sciences ◽

10.3390/ijms23020924 ◽

2022 ◽

Vol 23 (2) ◽

pp. 924

Author(s):

Julia Hauptstein ◽

Leonard Forster ◽

Ali Nadernezhad ◽

Jürgen Groll ◽

Jörg Teßmar ◽

...

Keyword(s):

Hyaluronic Acid ◽

Growth Factors ◽

Growth Factor ◽

Transforming Growth Factor Beta ◽

Transforming Growth Factor ◽

Cartilage Regeneration ◽

Cartilaginous Tissues ◽

Dual Stage ◽

Tgf Β1

In 3D bioprinting for cartilage regeneration, bioinks that support chondrogenic development are of key importance. Growth factors covalently bound in non-printable hydrogels have been shown to effectively promote chondrogenesis. However, studies that investigate the functionality of tethered growth factors within 3D printable bioinks are still lacking. Therefore, in this study, we established a dual-stage crosslinked hyaluronic acid-based bioink that enabled covalent tethering of transforming growth factor-beta 1 (TGF‑β1). Bone marrow-derived mesenchymal stromal cells (MSCs) were cultured over three weeks in vitro, and chondrogenic differentiation of MSCs within bioink constructs with tethered TGF‑β1 was markedly enhanced, as compared to constructs with non-covalently incorporated TGF‑β1. This was substantiated with regard to early TGF‑β1 signaling, chondrogenic gene expression, qualitative and quantitative ECM deposition and distribution, and resulting construct stiffness. Furthermore, it was successfully demonstrated, in a comparative analysis of cast and printed bioinks, that covalently tethered TGF‑β1 maintained its functionality after 3D printing. Taken together, the presented ink composition enabled the generation of high-quality cartilaginous tissues without the need for continuous exogenous growth factor supply and, thus, bears great potential for future investigation towards cartilage regeneration. Furthermore, growth factor tethering within bioinks, potentially leading to superior tissue development, may also be explored for other biofabrication applications.

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MiR-216a-5p alleviates LPS-induced inflammation in the human bronchial epithelial cell by inhibition of TGF-β1 signaling via down-regulating TGFBR2

Allergologia et Immunopathologia ◽

10.15586/aei.v49i5.458 ◽

2021 ◽

Vol 49 (5) ◽

pp. 64-71

Author(s):

Shan Liu ◽

Jianjun Li ◽

Liya Hu

Keyword(s):

Growth Factor ◽

Transforming Growth Factor Beta ◽

Transforming Growth Factor ◽

Ectopic Expression ◽

Luciferase Assay ◽

Enzyme Linked Immunosorbent Assay ◽

Bronchial Epithelial ◽

Tnf Α ◽

Tgf Β1

Objective: Bronchopneumonia is a common respiratory infection disease and is the leading cause of hospitalization in children under 5 years of age. Inflammation is the primary response caused by bronchopneumonia. But the detailed underlying mechanism of inflammation in bronchopneumonia remains unclear. Therefore, this study focused on studying the effect of miR-216a-5p on inflammation induced by bronchopneumonia and investigate the potential mechanism underlying it.Methods: Human bronchial epithelial cells (BEAS-2B) were stimulated using lipopolysaccha-rides (LPS) to trigger bronchopneumonia in vitro. The production of interleukin (IL)-1β, IL-6, and Tumor necrosis factor (TNF)-α was measured using the enzyme-linked immunosorbent assay. The luciferase assay was conducted to explore the relationship between miR-216a-5p and TGFBR2. Quantitative real-time polymerase chain reaction and western blot were used to detect the gene expression.Results: miR-216a-5p gene expression decreased in BEAS-2B cells stimulated by LPS. Overexpression of miR-216a-5p suppressed the elevated levels of IL-1β, IL-6, and TNF-α induced by LPS. Transforming growth factor-beta receptor 2 (TGFBR2) proved to be a direct target of miR-216a-5p, and they negatively modulated TGFBR2 expression. In addition, overexpression of miR-216a-5p inhibited LPS-induced protein levels of TGFBR2,transforming growth factor (TGF)-β1, and phosphorylation of SMAD family member 2 (smad2),. This ectopic expression of miR-216a-5p was restored by overexpressed TGFBR2.Conclusion: miR-216a-5p was decreased in LPS-stimulated BEAS-2B cells. Overexpressed miR-216a-5p suppressed LPS-induced inflammation in BEAS-2B cells by inhibition of TGF-β1 signal-ing via down-regulating TGFBR2. miR-216a-5p may be a valuable target for anti-inflammation treatment in bronchopneumonia.

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Vitamin D in Different Stages of Type 2 Diabetic Nephropathy and its Correlation with Transforming Growth Factor Beta-1 (TGF-β1) –A Cross Sectional Study

Journal of Pharmaceutical Research International ◽

10.9734/jpri/2021/v33i50b33437 ◽

2021 ◽

pp. 141-147

Author(s):

Liji Kavuparambil ◽

Ashok Kumar Pammi ◽

T. K. Jithesh ◽

K. Shifa

Keyword(s):

Vitamin D ◽

Diabetic Nephropathy ◽

Growth Factor ◽

Transforming Growth Factor Beta ◽

Transforming Growth Factor ◽

Diabetic Patients ◽

Vitamin D Status ◽

Cross Sectional ◽

Growth Factor Beta ◽

Tgf Β1

Background: Diabetic nephropathy (DN) is a microvascular complication of Diabetes Mellitus (DM) and the prevalence of which is increasing in every year. Monitoring of Vitamin D status in diabetic nephropathy patients is important, as the deficiency of vitamin D appears as a risk factor for the development of diabetic nephropathy. Studies evaluating the role of vitamin D in DN are few. Conflicting data is available on the correlation between vitamin D and Diabetic Nephropathy. Studies revealed the sample population is Vitamin D deficient. Therefore, it is important to understand the correlation of Vitamin D with severity of Diabetic nephropathy and its role in fibrogenesis. The aim of this study is to analyse vitamin D status in different stages of type 2 diabetic nephropathy and its correlation with transforming growth factor beta-1. Methods: A 1.5-year cross-sectional study of 120 diabetic patients, 60 with nephropathy and 60 without nephropathy patients enrolled to MES Medical College. Patients with heart, liver, or thyroid disease, as well as those on dialysis, were excluded from the study. The VITROS 5600 integrated system were used to measure fasting blood sugar (FBS), HbA1c, creatinine and vitamin D. Transforming Growth Factor Beta-1 (TGF-β1) is measured using ELISA technique. According to HbA1c and estimated glomerular filtration rate (eGFR) values, the study population is divided into two groups. The statistical package for the social sciences (SPSS) software was used to conduct the analysis. The level of significance was calculated at 95%. Results: The level of vitamin D in diabetic patients with nephropathy is much lower than in diabetic patients without nephropathy. In diabetic nephropathy patients, serum creatinine, urea, HbA1c and TGF-β1 exhibited a highly significant negative correlation with vitamin D status, but eGFR showed a highly significant positive correlation. Conclusion: Vitamin D status has been found to be poor in all diabetic patients, with a greater drop in diabetic nephropathy patients. In diabetic nephropathy patients, serum creatinine, urea, HbA1c and TGF-β1 exhibited a highly significant negative association with vitamin D status, but eGFR showed a highly significant positive link. Deficiency of vitamin D have role in the development and severity of DN, and showed a highly significant correlation with the regulator of fibrosis, TGF-β1. This finding indicates that vitamin D couldbe an important factor for development and progression of Diabetic nephropathy. So supplementation of vitamin D may slow down progression of DN.

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Platelet-Rich Plasma Prevents In Vitro Transforming Growth Factor-β1-Induced Fibroblast to Myofibroblast Transition: Involvement of Vascular Endothelial Growth Factor (VEGF)-A/VEGF Receptor-1-Mediated Signaling †

Cells ◽

10.3390/cells7090142 ◽

2018 ◽

Vol 7 (9) ◽

pp. 142 ◽

Cited By ~ 8

Author(s):

Flaminia Chellini ◽

Alessia Tani ◽

Larissa Vallone ◽

Daniele Nosi ◽

Paola Pavan ◽

...

Keyword(s):

Vascular Endothelial Growth Factor ◽

Growth Factor ◽

Transforming Growth Factor ◽

Platelet Rich Plasma ◽

Vegf Receptor ◽

Vascular Endothelial ◽

Endothelial Growth Factor ◽

The Impact ◽

Tgf Β1

The antifibrotic potential of platelet-rich plasma (PRP) is controversial. This study examined the effects of PRP on in vitro transforming growth factor (TGF)-β1-induced differentiation of fibroblasts into myofibroblasts, the main drivers of fibrosis, and the involvement of vascular endothelial growth factor (VEGF)-A in mediating PRP-induced responses. The impact of PRP alone on fibroblast differentiation was also assessed. Myofibroblastic phenotype was evaluated by confocal fluorescence microscopy and western blotting analyses of α-smooth muscle actin (sma) and type-1 collagen expression, vinculin-rich focal adhesion clustering, and stress fiber assembly. Notch-1, connexin 43, and VEGF-A expression were also analyzed by RT-PCR. PRP negatively regulated fibroblast-myofibroblast transition via VEGF-A/VEGF receptor (VEGFR)-1-mediated inhibition of TGF-β1/Smad3 signaling. Indeed TGF-β1/PRP co-treated fibroblasts showed a robust attenuation of the myofibroblastic phenotype concomitant with a decrease of Smad3 expression levels. The VEGFR-1 inhibition by KRN633 or blocking antibodies, or VEGF-A neutralization in these cells prevented the PRP-promoted effects. Moreover PRP abrogated the TGF-β1-induced reduction of VEGF-A and VEGFR-1 cell expression. The role of VEGF-A signaling in counteracting myofibroblast generation was confirmed by cell treatment with soluble VEGF-A. PRP as single treatment did not induce fibroblast myodifferentiation. This study provides new insights into cellular and molecular mechanisms underpinning PRP antifibrotic action.

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