Animal Models for Studying Soft Tissue Biocompatibility of Biomaterials
Yuehuei H. An, Richard J. Friedman in Animal Models in Orthopaedic Research, 2020
At approximately the third day, formation of collagen fibres by the fibroblasts becomes histologically visible.22 In addition, a network of capillaries is formed to provide oxygen to support the fibroblast synthesis of collagen. In front of the newly formed collagen matrix, the macrophages still continue to phagocytize the dead material hereby creating an environment for other fibroblasts to settle. This process continues until the wound is completely closed. The tissue formed is called granulation tissue. Already at the sixth day of wound healing, maturation of the collagen fibres starts. By means of collagen synthesis and lysis, remodelling of the collagen network occurs. Meanwhile, myofibroblasts are responsible for wound contraction, hereby reducing the wound surface. Finally, the number of cells will decrease, leaving scar tissue behind. The functional characteristics of this newly formed tissue are less effective compared to the original tissue, The wound strength will never reach its original value and scar tissue is nonelastic.22-24
Anterior retinectomy
A Peyman MD Gholam, A Meffert MD Stephen, D Conway MD FACS Mandi, Chiasson Trisha in Vitreoretinal Surgical Techniques, 2019
The pathogenesis of this proliferative tissue is believed to be derived from retinal pigment epithelial (RPE) cells that are liberated at the time of the original retinal detachment or its repair.7,8 The RPE cells presumably undergo fibroblastic transformation, with the ability to synthesize collagen and transform into macrophages. The fibroblasts arise from myofibroblasts; they contract and form mature fibrocytes, fixing the tissue. These cells can cause retraction of the retina and vitreous body, leading to recurrent retinal detachment. The proliferative membranes, similar to those seen in proliferative vascular and diabetic retinopathy, can cause extensive contraction. Despite aggressive membrane dissection, the effective retinal foreshortening still may prevent reapproximation of the retina to the underlying RPE.
Pathogenesis
Aparna Palit, Arun C. Inamadar in Systemic Sclerosis, 2019
The differentiation of fibroblasts into myofibroblasts or activated fibroblasts is very crucial in the pathogenesis of SSc, as these cells produce ECM proteins at a higher rate. The presence of alpha-Smooth Muscle Actin (SMA) indicates a myofibroblast population. TGF-β mediates the selection of the higher number of alpha SMA positive and apoptosis resistant fibroblasts. TGF-β acts as chemoattractant to fibroblasts and protects myofibroblasts from undergoing apoptosis. TGF-β inhibits the upregulation of inducible NO synthase, a mediator of apoptosis, in IL-1 stimulated fibroblasts. The apoptosis of fibroblasts through Fas (CD95/Apo-1) signaling is also inhibited by TGF-β. Insulin-like growth factor (IGF)-1 is known to reduce non-Fas mediated apoptosis through starvation in glomerular mesangial cells, which are similar to dermal fibroblasts.
Optimization of process parameters for fabrication of electrospun nanofibers containing neomycin sulfate and Malva sylvestris extract for a better diabetic wound healing
Published in Drug Delivery, 2022
Mohammed Monirul Islam, Varshini HR, Penmetsa Durga Bhavani, Prakash S. Goudanavar, N. Raghavendra Naveen, B. Ramesh, Santosh Fattepur, Predeepkumar Narayanappa Shiroorkar, Mohammed Habeebuddin, Girish Meravanige, Mallikarjun Telsang, Nagaraja Sreeharsha
In addition, the size of wounds treated with an extract containing nanofibers was reduced. By day 14, the percentage of wounds treated with NS-NF and MS-NS-NF was found to be 89.64% and 96.08%, respectively, compared to 56.84% of wound healing in the control group. Wound contraction occurs throughout the healing phase owing to the proliferation of fibroblasts induced by contractile myofibroblasts. In accordance with the findings of the release and anti-bacterial tests, the proportion of wounds that healed in MS-NS-NF samples was found to be quite similar. Sustaining medication release after a successful first burst release is extremely desirable for the treatment of both the original and most recent wound infection (Rath et al., 2016b). On day 7, some inflammatory responses were reported for gauze-treated lesions. Blood vessels and granulation tissues were seen in the wounds treated with MS-NS-NF. Also evident was the development of fibroblast cells.
Hyalocytes in proliferative vitreo-retinal diseases
Published in Expert Review of Ophthalmology, 2022
Charlotte H. Jones, Wei Gui, Ricarda G. Schumann, Stefaniya K. Boneva, Clemens A. K. Lange, Koen A. van Overdam, Toco Y. P. Chui, Richard B. Rosen, Michael Engelbert, J. Sebag
Myofibroblasts are the contractile components of fibrocellular membranes. Their contractile properties and their ability to produce newly formed collagen have been demonstrated in numerous studies of the diabetic vitreo-retinal interface [68,87]. In particular, ultrastructural analyses of the co-localization α-SMA filaments and collagen type I and III proved the presence of hyalocytes in fibrocellular membranes of diabetic eyes [84]. Hyalocytes and myofibroblasts are usually embedded in thick layers of native vitreous collagen. In addition, newly-formed collagen and fibrous long-spacing collagen were seen in diabetic retinopathy representing a remodeling process of vitreous cortex collagen [79,84,88]. Pathologic changes at the vitreo-macular interface were present in all eyes irrespective of the presence of tractional fibrocellular membranes.
RhoA/ROCK Signaling Regulates TGF-β1-Induced Fibrotic Effects in Human Pterygium Fibroblasts through MRTF-A
Published in Current Eye Research, 2022
Jiajun Xie, Qingyao Ning, Huina Zhang, Shuang Ni, Juan Ye
Excessive wound healing after surgical excision often leads to fibrosis, including myofibroblast activation and extracellular matrix (ECM) remodeling, which indicates the recurrence of pterygium. Alpha smooth muscle actin (α-SMA) is a key marker of myofibroblasts.10 Myofibroblasts rapidly synthesize and accumulate redundant amounts of ECM, including collagen I, III, and secrete metalloproteinases (MMPs) thus transforming the site into a chronic wound.11,12 Transforming growth factor-beta 1 (TGF-β1) has been identified as a primary inducer of fibrosis in the pathogenesis and progression of pterygium.13 The overexpression of TGF-β1 was observed in pterygium tissues compared to normal conjunctiva,14 and in the same way in recurrent pterygium fibroblast cultures compared with primary pterygium fibroblast cultures.15 Since TGF-β1 and its downstream signaling are involved in the pathogenesis and progression of pterygium, TGF-β1 was used to induce fibrosis in human pterygium fibroblasts (HPFs) in the present study.
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