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      TGF-β1 Effects on Total Collagen of the New Zealand Rabbit’s Urethral Wall (Oryctolagus cuniculus) in Animal Models of Urethral Stricture

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          Abstract

          Background:

          Currently, animal models of urethral stricture are not standardized. Transforming Growth Factor Beta 1 (TGF-β1) regulates extracellular matrix deposition in homeostatic and pathological responses.

          Objective:

          The aim of this study was to present the potential model to be developed as a urethral stricture.

          Methods:

          True experimental laboratory research was conducted by using Male New Zealand rabbits ( Oryctolagus cuniculus), which were divided into 5 groups; control, placebo, and 3 treatment groups (TGF-β1 injection of 1 µg, 2 µg, 4 µg). Urethrography, histopathological analysis, and evaluation of total collagen formation of the urethral wall were performed after 6 weeks.

          Results:

          An increase in the dose of TGF-β1 decreased the mean rabbit’s urethral lumen diameter (29.3% in the 2µg group and 34% in the 4µg group) compared to controls. Three rabbits decreased as much as ≤ 50% in urethral lumen diameter. Significant increases in total collagen density in the periluminal and peripheral urethral spongiosum were noted by increasing doses of TGF-β1. The percentage of urethral lumen diameter has a strong negative correlation with periluminal total collagen density (r = -0,798; p = 0,000) and very strong negative correlation with peripheral spongiosa total collagen density (r = -0,748, p = 0,000).

          Conclusion:

          TGF-β1 plays a role in changing total collagen compositions of the rabbit’s urethral wall, decreasing the urethral lumen diameter. Further research with increasing doses of TGF-β1 is needed to determine the effective dose of TGF-β1 in inducing urethral stricture.

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          Most cited references13

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          Mechanisms of fibrosis: therapeutic translation for fibrotic disease.

          Fibrosis is a pathological feature of most chronic inflammatory diseases. Fibrosis, or scarring, is defined by the accumulation of excess extracellular matrix components. If highly progressive, the fibrotic process eventually leads to organ malfunction and death. Fibrosis affects nearly every tissue in the body. Here we discuss how key components of the innate and adaptive immune response contribute to the pathogenesis of fibrosis. We also describe how cell-intrinsic changes in important structural cells can perpetuate the fibrotic response by regulating the differentiation, recruitment, proliferation and activation of extracellular matrix-producing myofibroblasts. Finally, we highlight some of the key mechanisms and pathways of fibrosis that are being targeted as potential therapies for a variety of important human diseases.
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            • Record: found
            • Abstract: found
            • Article: not found

            TGF-beta and TNF-alpha: antagonistic cytokines controlling type I collagen gene expression.

            The balance between production and degradation of type I collagen plays a critical role in the development and maintenance of organ and tissue integrity. It also represents the most crucial element governing the process of tissue repair. The synthesis of type I collagen gene is highly regulated by different cytokines at the transcriptional level. Especially, transforming growth factor beta (TGF-beta), a key player in the physiopathology of tissue repair, enhances type I collagen gene expression. In contrast, tumor necrosis factor alpha (TNF-alpha), whose matrix-remodelling function is opposite to that of TGF-beta, reduces type I collagen gene expression. This review focuses on transcriptional regulation of type I collagen by TGF-beta and TNF-alpha and on the molecular mechanisms that control the antagonistic activity of TNF-alpha against TGF-beta-driven type I collagen gene expression.
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              • Record: found
              • Abstract: not found
              • Article: not found

              The controversial role of tumor necrosis factor alpha in fibrotic diseases.

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                Author and article information

                Journal
                Med Arch
                Med Arch
                Medical Archives
                Medical Archives
                Academy of Medical Sciences of Bosnia and Herzegovina
                0350-199X
                1986-5961
                2023
                : 77
                : 3
                : 189-193
                Affiliations
                [1 ]Doctoral Program in Medical Science, Faculty of Medicine Universitas Brawijaya, Malang, Indonesia
                [2 ]Department of Urology, Faculty of Medicine Universitas Brawijaya – Saiful Anwar General Hospital, Malang, Indonesia
                [3 ]Department of Pathology Anatomy, Faculty of Medicine Universitas Brawijaya – Saiful Anwar General Hospital, Malang, Indonesia
                [4 ]Department of Radiology, Faculty of Medicine Universitas Brawijaya – Saiful Anwar General Hospital, Malang, Indonesia
                [5 ]Department of Biochemistry, Faculty of Medicine, Universitas Brawijaya, Malang, Indonesia
                Author notes
                Corresponding author: Paksi Satyagraha.Doctoral Program in Medical Science, Faculty of Medicine Universitas Brawijaya, Malang, Indonesia. uropas.fk@ 123456ub.ac.id . ORCID ID: http//www.orcid.org/0000-0002-9174-2629.
                Article
                10.5455/medarh.2023.77.189-193
                10495137
                37700922
                f7f0a936-d1cb-4876-bd04-c38bb6b23b41
                © 2023 Paksi Satyagraha, Hamid Hunaif Dhofi Alluza,I Made Udiyana Indradiputra, Athaya Febriantyo Purnomo, Pradana Nurhadi, Kenty Wantri Anita, Yuyun Yueniwati, Happy Kurnia Permatasari, Basuki Bambang Purnomo

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 06 April 2023
                : 10 May 2023
                Categories
                Original Paper

                tgf-β1,urethral stricture,total collagen
                tgf-β1, urethral stricture, total collagen

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