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Journal articles on the topic 'Myofibroblasrts'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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1

Poobalarahi, Felicitta, Catalin F. Baicu, and Amy D. Bradshaw. "Cardiac myofibroblasts differentiated in 3D culture exhibit distinct changes in collagen I production, processing, and matrix deposition." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 6 (2006): H2924—H2932. http://dx.doi.org/10.1152/ajpheart.00153.2006.

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Myofibroblasts are a differentiated fibroblast cell type characterized by increased contractile capacity and elevated production of extracellular matrix (ECM) proteins. In the heart, myofibroblast expression is implicated in fibrosis associated with pressure-overload hypertrophy, among other pathologies. Although enhanced expression of ECM proteins by myofibroblasts is established, few studies have addressed the nature of the ECM deposited by myofibroblasts. To characterize ECM production and assembly by cardiac myofibroblasts, we developed a three-dimensional (3D) culture system using primary

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Lapthorn, Alice, Marcus Ilg, Justine Sullivan, Peter Dziewulski, and Selim Cellek. "P03 Hydroxypyridone antifungals induce myofibroblast apoptosis in an in vitro model of hypertrophic scars." British Journal of Dermatology 189, no. 1 (2023): e15-e15. http://dx.doi.org/10.1093/bjd/ljad174.025.

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Abstract Despite being the most common complication following burn injury, there are no medications to prevent the formation of hypertrophic scars. Myofibroblasts are key cells involved in scar formation, responsible for producing excessive amounts of extracellular matrix and have been shown to be resistant to apoptosis. We have previously shown that hydroxypyridone antifungals can inhibit the transformation of fibroblasts to myofibroblasts, and exhibit other antifibrotic effects. This study aimed to investigate the effect of these drugs on established myofibroblasts. Primary human dermal fibr

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Wipff, Pierre-Jean, Daniel B. Rifkin, Jean-Jacques Meister та Boris Hinz. "Myofibroblast contraction activates latent TGF-β1 from the extracellular matrix". Journal of Cell Biology 179, № 6 (2007): 1311–23. http://dx.doi.org/10.1083/jcb.200704042.

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The conjunctive presence of mechanical stress and active transforming growth factor β1 (TGF-β1) is essential to convert fibroblasts into contractile myofibroblasts, which cause tissue contractures in fibrotic diseases. Using cultured myofibroblasts and conditions that permit tension modulation on the extracellular matrix (ECM), we establish that myofibroblast contraction functions as a mechanism to directly activate TGF-β1 from self-generated stores in the ECM. Contraction of myofibroblasts and myofibroblast cytoskeletons prepared with Triton X-100 releases active TGF-β1 from the ECM. This pro

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Haas, MaryEllen R., Darlene V. Nguyen, and Brett A. Shook. "Recovery of Altered Diabetic Myofibroblast Heterogeneity and Gene Expression Are Associated with CD301b+ Macrophages." Biomedicines 9, no. 12 (2021): 1752. http://dx.doi.org/10.3390/biomedicines9121752.

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Diabetic wound healing is associated with impaired function and reduced numbers of myofibroblasts, a heterogeneous cell population with varying capacities to promote repair. To determine how diabetes alters myofibroblast composition, we performed flow cytometry and spatial tissue analysis of myofibroblast subsets throughout the healing process in diabetic (db/db) and control (db/+) mouse skin. We observed reduced numbers of profibrotic SCA1+; CD34+; CD26+ myofibroblasts in diabetic wounds five days after injury, with decreased expression of fibrosis-associated genes compared to myofibroblasts

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Mewhort, Holly E. M., Brodie D. Lipon, Daniyil A. Svystonyuk та ін. "Monocytes increase human cardiac myofibroblast-mediated extracellular matrix remodeling through TGF-β1". American Journal of Physiology-Heart and Circulatory Physiology 310, № 6 (2016): H716—H724. http://dx.doi.org/10.1152/ajpheart.00309.2015.

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Following myocardial infarction (MI), cardiac myofibroblasts remodel the extracellular matrix (ECM), preventing mechanical complications. However, prolonged myofibroblast activity leads to dysregulation of the ECM, maladaptive remodeling, fibrosis, and heart failure (HF). Chronic inflammation is believed to drive persistent myofibroblast activity; however, the mechanisms are unclear. We assessed the influence of peripheral blood monocytes on human cardiac myofibroblast activity in a three-dimensional (3D) ECM microenvironment. Human cardiac myofibroblasts isolated from surgical biopsies of the

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Rice, Nancy A., and Leslie A. Leinwand. "Skeletal myosin heavy chain function in cultured lung myofibroblasts." Journal of Cell Biology 163, no. 1 (2003): 119–29. http://dx.doi.org/10.1083/jcb.200303194.

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Myofibroblasts are unique contractile cells with both muscle and nonmuscle properties. Typically myofibroblasts are identified by the expression of α smooth muscle actin (ASMA); however some myofibroblasts also express sarcomeric proteins. In this study, we show that pulmonary myofibroblasts express three of the eight known sarcomeric myosin heavy chains (MyHCs) (IIa, IId, and embryonic) and that skeletal muscle myosin enzymatic activity is required for pulmonary myofibroblast contractility. Furthermore, inhibition of skeletal myosin activity and myofibroblast contraction results in a decrease

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Baum, Jennifer R., Biao Long, Candido Cabo, and Heather S. Duffy. "Myofibroblasts cause heterogeneous Cx43 reduction and are unlikely to be coupled to myocytes in the healing canine infarct." American Journal of Physiology-Heart and Circulatory Physiology 302, no. 3 (2012): H790—H800. http://dx.doi.org/10.1152/ajpheart.00498.2011.

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Following myocardial infarction (MI) inflammatory responses transform cardiac fibroblasts to myofibroblasts, which in vitro studies show form heterocellular gap junctions with cardiac myocytes via Connexin43 (Cx43). The ability to form heterocellular junctions in the intact heart and the impact of these junctions on propagation is unclear. We used a canine model of MI and characterized the distribution and quantity of myofibroblasts in surviving epicardial cells [epicardial border zone (EBZ)]. We found a significant increase in myofibroblasts within the EBZ and no gap junction plaques between

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Sánchez, Jorge, Beatriz Trenor, Javier Saiz, Olaf Dössel, and Axel Loewe. "Fibrotic Remodeling during Persistent Atrial Fibrillation: In Silico Investigation of the Role of Calcium for Human Atrial Myofibroblast Electrophysiology." Cells 10, no. 11 (2021): 2852. http://dx.doi.org/10.3390/cells10112852.

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During atrial fibrillation, cardiac tissue undergoes different remodeling processes at different scales from the molecular level to the tissue level. One central player that contributes to both electrical and structural remodeling is the myofibroblast. Based on recent experimental evidence on myofibroblasts’ ability to contract, we extended a biophysical myofibroblast model with Ca2+ handling components and studied the effect on cellular and tissue electrophysiology. Using genetic algorithms, we fitted the myofibroblast model parameters to the existing in vitro data. In silico experiments show

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Lodyga, Monika, Elizabeth Cambridge, Henna M. Karvonen та ін. "Cadherin-11–mediated adhesion of macrophages to myofibroblasts establishes a profibrotic niche of active TGF-β". Science Signaling 12, № 564 (2019): eaao3469. http://dx.doi.org/10.1126/scisignal.aao3469.

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Macrophages contribute to the activation of fibroblastic cells into myofibroblasts, which secrete collagen and contract the collagen matrix to acutely repair injured tissue. Persistent myofibroblast activation leads to the accumulation of fibrotic scar tissue that impairs organ function. We investigated the key processes that turn acute beneficial repair into destructive progressive fibrosis. We showed that homotypic cadherin-11 interactions promoted the specific binding of macrophages to and persistent activation of profibrotic myofibroblasts. Cadherin-11 was highly abundant at contacts betwe

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Honey, Nafzia, and Niroshini Rajaram. "The Dynamic Role Of Myofibroblasts In Oral Tissue Homeostasis And Disease." International Journal of Histopathological Interpretation 13, no. 1 (2024): 11–16. http://dx.doi.org/10.56501/intjhistopatholinterpret.v13i1.1047.

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Myofibroblasts are specialized cells that play a crucial role in maintaining the structural integrity and function of oral tissues. These cells exhibit a unique phenotype marked by the expression of alpha-smooth muscle actin (α-SMA), and possess the ability to contract and produce extracellular matrix components. In healthy oral tissues, myofibroblasts contribute to tissue homeostasis by mediating wound healing, tissue remodeling, and matrix turnover. However, the dysregulation of myofibroblast function can lead to pathological conditions such as fibrosis, scarring, and oral cancer. This revie

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Tai, Yifan, Emma L. Woods, Jordanna Dally, et al. "Myofibroblasts: Function, Formation, and Scope of Molecular Therapies for Skin Fibrosis." Biomolecules 11, no. 8 (2021): 1095. http://dx.doi.org/10.3390/biom11081095.

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Myofibroblasts are contractile, α-smooth muscle actin-positive cells with multiple roles in pathophysiological processes. Myofibroblasts mediate wound contractions, but their persistent presence in tissues is central to driving fibrosis, making them attractive cell targets for the development of therapeutic treatments. However, due to shared cellular markers with several other phenotypes, the specific targeting of myofibroblasts has long presented a scientific and clinical challenge. In recent years, myofibroblasts have drawn much attention among scientific research communities from multiple d

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Hsia, Lin-ting, Neil Ashley, Djamila Ouaret, Lai Mun Wang, Jennifer Wilding, and Walter F. Bodmer. "Myofibroblasts are distinguished from activated skin fibroblasts by the expression of AOC3 and other associated markers." Proceedings of the National Academy of Sciences 113, no. 15 (2016): E2162—E2171. http://dx.doi.org/10.1073/pnas.1603534113.

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Pericryptal myofibroblasts in the colon and rectum play an important role in regulating the normal colorectal stem cell niche and facilitating tumor progression. Myofibroblasts previously have been distinguished from normal fibroblasts mostly by the expression of α smooth muscle actin (αSMA). We now have identified AOC3 (amine oxidase, copper containing 3), a surface monoamine oxidase, as a new marker of myofibroblasts by showing that it is the target protein of the myofibroblast-reacting mAb PR2D3. The normal and tumor tissue distribution and the cell line reactivity of AOC3 match that expect

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Bernstein, Audrey M., Sally S. Twining, Debra J. Warejcka, Edward Tall, and Sandra K. Masur. "Urokinase Receptor Cleavage: A Crucial Step in Fibroblast-to-Myofibroblast Differentiation." Molecular Biology of the Cell 18, no. 7 (2007): 2716–27. http://dx.doi.org/10.1091/mbc.e06-10-0912.

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Fibroblasts migrate into and repopulate connective tissue wounds. At the wound edge, fibroblasts differentiate into myofibroblasts, and they promote wound closure. Regulated fibroblast-to-myofibroblast differentiation is critical for regenerative healing. Previous studies have focused on the role in fibroblasts of urokinase plasmingen activator/urokinase plasmingen activator receptor (uPA/uPAR), an extracellular protease system that promotes matrix remodeling, growth factor activation, and cell migration. Whereas fibroblasts have substantial uPA activity and uPAR expression, we discovered that

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BISSON, M. A., D. A. MCGROUTHER, V. MUDERA та A. O. GROBBELAAR. "The Different Characteristics of Dupuytren’s Disease Fibroblasts Derived from Either Nodule or Cord: Expression of α-Smooth Muscle Actin and the Response to Stimulation by TGF-β1". Journal of Hand Surgery 28, № 4 (2003): 351–56. http://dx.doi.org/10.1016/s0266-7681(03)00135-9.

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Mechanisms behind the onset and progression of Dupuytren’s disease are poorly understood. Both myofibroblasts and transforming growth factor beta 1 (TGF-β1) have been implicated. We studied fibroblast cultures derived from nodules or cords of Dupuytren’s contracture tissue to determine the proportion of myofibroblasts present in comparison with flexor retinaculum fibroblast cultures. We identified myofibroblasts by immunohistochemical staining for α-SMA. We then investigated the effects of TGF-β1 stimulation on these fibroblasts. Basal myofibroblast/fibroblast proportions were 9.7% in nodule c

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Pho, M., W. Lee, D. R. Watt, C. Laschinger, C. A. Simmons, and C. A. McCulloch. "Cofilin is a marker of myofibroblast differentiation in cells from porcine aortic cardiac valves." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 4 (2008): H1767—H1778. http://dx.doi.org/10.1152/ajpheart.01305.2007.

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The formation of myofibroblasts in valve interstitial cell (VIC) populations contributes to fibrotic valvular disease. We examined myofibroblast differentiation in VICs from porcine aortic valves. In normal valves, cells immunostained for α-smooth muscle actin (α-SMA, a myofibroblast marker) were rare (0.69 ± 0.48%), but in sclerotic valves of animals fed an atherogenic diet, myofibroblasts were spatially clustered and abundant (31.2 ± 6.3%). In cultured VIC populations from normal valves, SMA-positive myofibroblasts were also spatially clustered, abundant (21% positive cells after 1 passage),

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Yan, Mengchao, Ye Xie, Jia Yao, and Xun Li. "The Dual-Mode Transition of Myofibroblasts Derived from Hepatic Stellate Cells in Liver Fibrosis." International Journal of Molecular Sciences 24, no. 20 (2023): 15460. http://dx.doi.org/10.3390/ijms242015460.

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Hepatic stellate cells (HSCs) are the key promoters of liver fibrosis. In response to liver-fibrosis-inducing factors, HSCs express alpha smooth muscle actin (α-SMA) and obtain myofibroblast phenotype. Collagen secretion and high expression of α-SMA with related high cell tension and migration limitation are the main characteristics of myofibroblasts. How these two characteristics define the role of myofibroblasts in the initiation and progression of liver fibrosis is worth exploring. From this perspective, we explored the correlation between α-SMA expression and collagen secretion in myofibro

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Shook, Brett A., Renee R. Wasko, Guillermo C. Rivera-Gonzalez, et al. "Myofibroblast proliferation and heterogeneity are supported by macrophages during skin repair." Science 362, no. 6417 (2018): eaar2971. http://dx.doi.org/10.1126/science.aar2971.

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During tissue repair, myofibroblasts produce extracellular matrix (ECM) molecules for tissue resilience and strength. Altered ECM deposition can lead to tissue dysfunction and disease. Identification of distinct myofibroblast subsets is necessary to develop treatments for these disorders. We analyzed profibrotic cells during mouse skin wound healing, fibrosis, and aging and identified distinct subpopulations of myofibroblasts, including adipocyte precursors (APs). Multiple mouse models and transplantation assays demonstrate that proliferation of APs but not other myofibroblasts is activated by

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Walsh, Sinead M., Julie C. Worrell, Aurelie Fabre, Boris Hinz, Rosemary Kane, and Michael P. Keane. "Novel differences in gene expression and functional capabilities of myofibroblast populations in idiopathic pulmonary fibrosis." American Journal of Physiology-Lung Cellular and Molecular Physiology 315, no. 5 (2018): L697—L710. http://dx.doi.org/10.1152/ajplung.00543.2017.

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Idiopathic pulmonary fibrosis (IPF), a chronic progressive interstitial pneumonia, is characterized by excessive fibroproliferation. Key effector cells in IPF are myofibroblasts that are recruited from three potential sources: resident fibroblasts, fibrocytes, and epithelial cells. We hypothesized that IPF myofibroblasts from different sources display unique gene expression differences and distinct functional characteristics. Primary human pulmonary fibroblasts (normal and IPF), fibrocytes, and epithelial cells were activated using the profibrotic factors TGF-β and TNF-α. The resulting myofibr

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McKaig, Brian C., Shavcharn S. Makh, Christopher J. Hawkey, Daniel K. Podolsky та Yashwant R. Mahida. "Normal human colonic subepithelial myofibroblasts enhance epithelial migration (restitution) via TGF-β3". American Journal of Physiology-Gastrointestinal and Liver Physiology 276, № 5 (1999): G1087—G1093. http://dx.doi.org/10.1152/ajpgi.1999.276.5.g1087.

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-After injury and loss of epithelial cells, intestinal barrier function is reestablished by migration of viable epithelial cells from the wound edge (restitution). Myofibroblasts are located close to the basal surface of epithelial cells. This study aimed to investigate the role of human colonic subepithelial myofibroblasts in epithelial restitution. Primary cultures of subepithelial myofibroblasts were established. Monolayers of the epithelial cell lines IEC-6 and T84 were “wounded” in a standard manner to create an in vitro model of restitution. Migration of epithelial cells across the wound

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Bachamanda Somesh, Dipthi, Karsten Jürchott, Thomas Giesel, et al. "Microcurrent-Mediated Modulation of Myofibroblasts for Cardiac Repair and Regeneration." International Journal of Molecular Sciences 25, no. 6 (2024): 3268. http://dx.doi.org/10.3390/ijms25063268.

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Cardiovascular diseases are a significant cause of illness and death worldwide, often resulting in myofibroblast differentiation, pathological remodeling, and fibrosis, characterized by excessive extracellular matrix protein deposition. Treatment options for cardiac fibrosis that can effectively target myofibroblast activation and ECM deposition are limited, necessitating an unmet need for new therapeutic approaches. In recent years, microcurrent therapy has demonstrated promising therapeutic effects, showcasing its translational potential in cardiac care. This study therefore sought to invest

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van Beurden, H. E., J. W. Von den Hoff, R. Torensma, J. C. Maltha, and A. M. Kuijpers-Jagtman. "Myofibroblasts in Palatal Wound Healing: Prospects for the Reduction of Wound Contraction after Cleft Palate Repair." Journal of Dental Research 84, no. 10 (2005): 871–80. http://dx.doi.org/10.1177/154405910508401002.

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The surgical closure of orofacial clefts is considered to impair maxillary growth and dento-alveolar development. Wound contraction and subsequent scar tissue formation, during healing of these surgical wounds, contribute largely to these growth disturbances. The potential to minimize wound contraction and subsequent scarring by clinical interventions depends on the surgeon’s knowledge of the events responsible for these phenomena. Fibroblasts initiate wound contraction, but proto-myofibroblasts and mature myofibroblasts are by far the most important cells in this process. Myofibroblasts are c

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Hinz, B., P. Pittet, J. Smith-Clerc, C. Chaponnier, and J. J. Meister. "Myofibroblast Development Is Characterized by Specific Cell-Cell Adherens Junctions." Molecular Biology of the Cell 15, no. 9 (2004): 4310–20. http://dx.doi.org/10.1091/mbc.e04-05-0386.

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Myofibroblasts of wound granulation tissue, in contrast to dermal fibroblasts, join stress fibers at sites of cadherin-type intercellular adherens junctions (AJs). However, the function of myofibroblast AJs, their molecular composition, and the mechanisms of their formation are largely unknown. We demonstrate that fibroblasts change cadherin expression from N-cadherin in early wounds to OB-cadherin in contractile wounds, populated with α-smooth muscle actin (α-SMA)-positive myofibroblasts. A similar shift occurs during myofibroblast differentiation in culture and seems to be responsible for th

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Hinz, Boris, Vera Dugina, Christoph Ballestrem, Bernhard Wehrle-Haller та Christine Chaponnier. "α-Smooth Muscle Actin Is Crucial for Focal Adhesion Maturation in Myofibroblasts". Molecular Biology of the Cell 14, № 6 (2003): 2508–19. http://dx.doi.org/10.1091/mbc.e02-11-0729.

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Cultured myofibroblasts are characterized by stress fibers, containing α-smooth muscle actin (α-SMA) and by supermature focal adhesions (FAs), which are larger than FAs of α-SMA–negative fibroblasts. We have investigated the role of α-SMA for myofibroblast adhesion and FA maturation. Inverted centrifugation reveals two phases of initial myofibroblast attachment: during the first 2 h of plating microfilament bundles contain essentially cytoplasmic actin and myofibroblast adhesion is similar to that of α-SMA–negative fibroblasts. Then, myofibroblasts incorporate α-SMA in stress fibers, develop m

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Rozycki, Matthew, Monika Lodyga, Jessica Lam, et al. "The fate of the primary cilium during myofibroblast transition." Molecular Biology of the Cell 25, no. 5 (2014): 643–57. http://dx.doi.org/10.1091/mbc.e13-07-0429.

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Myofibroblasts, the culprit of organ fibrosis, can originate from mesenchymal and epithelial precursors through fibroblast–myofibroblast and epithelial–myofibroblast transition (EMyT). Because certain ciliopathies are associated with fibrogenesis, we sought to explore the fate and potential role of the primary cilium during myofibroblast formation. Here we show that myofibroblast transition from either precursor results in the loss of the primary cilium. During EMyT, initial cilium growth is followed by complete deciliation. Both EMyT and cilium loss require two-hit conditions: disassembly/abs

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WONG, M., та V. MUDERA. "Feedback Inhibition of High TGF-β1 Concentrations on Myofibroblast Induction and Contraction by Dupuytren’s Fibroblasts". Journal of Hand Surgery 31, № 5 (2006): 473–83. http://dx.doi.org/10.1016/j.jhsb.2006.05.007.

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Myofibroblasts and TGF-β1 are implicated in Dupuytren’s contracture. Transforming growth factor β1(TGF-β1) (1–10 ng/ml) increases myofibroblast induction in Dupuytren’s fibroblasts and contraction in a collagen model. However, higher doses (20–30 ng/ml) inhibit contraction in dermal fibroblasts. We hypothesized higher doses of TGF-β1 would inhibit induction of myofibroblasts and contraction by Dupuytren’s fibroblasts. Increasing doses of TGF-β1 (0–30 ng/ml) were tested on Dupuytren’s fibroblasts using immunofluorescence to determine myofibroblast upregulation and a 3D collagen model used to de

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McKaig, B. C., K. Hughes, P. J. Tighe та Y. R. Mahida. "Differential expression of TGF-β isoforms by normal and inflammatory bowel disease intestinal myofibroblasts". American Journal of Physiology-Cell Physiology 282, № 1 (2002): C172—C182. http://dx.doi.org/10.1152/ajpcell.00048.2001.

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First published September 5, 2001; 10.1152/ajpcell. 00048.2001.—Intestinal strictures are frequent in Crohn's disease but not ulcerative colitis. We investigated the expression of transforming growth factor (TGF)-β isoforms by isolated and cultured primary human intestinal myofibroblasts and the responsiveness of these cells and intestinal epithelial cells to TGF-β isoforms. Normal intestinal myofibroblasts released predominantly TGF-β3 and ulcerative colitis myofibroblasts expressed both TGF-β1 and TGF-β3, whereas in myofibroblast cultures from fibrotic Crohn's disease tissue, there was signi

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Cohen, Pazit Y., Raphael Breuer, Philip Zisman, and Shulamit B. Wallach-Dayan. "Bleomycin-Treated Chimeric Thy1-Deficient Mice with Thy1-Deficient Myofibroblasts and Thy-Positive Lymphocytes Resolve Inflammation without Affecting the Fibrotic Response." Mediators of Inflammation 2015 (2015): 1–13. http://dx.doi.org/10.1155/2015/942179.

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Lung fibrosis is characterized by abnormal accumulation of fibroblasts in the interstitium of the alveolar space. Two populations of myofibroblasts, distinguished by Thy1 expression, are detected in human and murine lungs. Accumulation of Thy1-negative (Thy1−) myofibroblasts was shown in the lungs of humans with idiopathic pulmonary fibrosis (IPF) and of bleomycin-treated mice. We aimed to identify genetic changes in lung myofibroblasts following Thy1 crosslinking and assess the impact of specific lung myofibroblast Thy1-deficiency, in vivo, in bleomycin-injured mouse lungs. Thy1 increased in

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Bochaton-Piallat, Marie-Luce, Giulio Gabbiani, and Boris Hinz. "The myofibroblast in wound healing and fibrosis: answered and unanswered questions." F1000Research 5 (April 26, 2016): 752. http://dx.doi.org/10.12688/f1000research.8190.1.

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The discovery of the myofibroblast has allowed definition of the cell responsible for wound contraction and for the development of fibrotic changes. This review summarizes the main features of the myofibroblast and the mechanisms of myofibroblast generation. Myofibroblasts originate from a variety of cells according to the organ and the type of lesion. The mechanisms of myofibroblast contraction, which appear clearly different to those of smooth muscle cell contraction, are described. Finally, we summarize the possible strategies in order to reduce myofibroblast activities and thus influence s

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Dwivedi, Nidhi, Shixin Tao, Abeda Jamadar, et al. "Epithelial Vasopressin Type-2 Receptors Regulate Myofibroblasts by a YAP-CCN2–Dependent Mechanism in Polycystic Kidney Disease." Journal of the American Society of Nephrology 31, no. 8 (2020): 1697–710. http://dx.doi.org/10.1681/asn.2020020190.

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BackgroundFibrosis is a major cause of loss of renal function in autosomal dominant polycystic kidney disease (ADPKD). In this study, we examined whether vasopressin type-2 receptor (V2R) activity in cystic epithelial cells can stimulate interstitial myofibroblasts and fibrosis in ADPKD kidneys.MethodsWe treated Pkd1 gene knockout (Pkd1KO) mice with dDAVP, a V2R agonist, for 3 days and evaluated the effect on myofibroblast deposition of extracellular matrix (ECM). We also analyzed the effects of conditioned media from primary cultures of human ADPKD cystic epithelial cells on myofibroblast act

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Freed, Darren H., Lisa Chilton, Yun Li, et al. "Role of myosin light chain kinase in cardiotrophin-1-induced cardiac myofibroblast cell migration." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 2 (2011): H514—H522. http://dx.doi.org/10.1152/ajpheart.01041.2010.

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Chemotactic movement of myofibroblasts is recognized as a common means for their sequestration to the site of tissue injury. Following myocardial infarction (MI), recruitment of cardiac myofibroblasts to the infarct scar is a critical step in wound healing. Contractile myofibroblasts express embryonic smooth muscle myosin, α-smooth muscle actin, as well as collagens I and III. We examined the effects of cardiotrophin-1 (CT-1) in the induction of primary rat ventricular myofibroblast motility. Changes in membrane potential (Em) and Ca2+entry were studied to reveal the mechanisms for induction o

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Mifflin, R. C., I. V. Pinchuk, J. I. Saada, and D. W. Powell. "Intestinal myofibroblasts: targets for stem cell therapy." American Journal of Physiology-Gastrointestinal and Liver Physiology 300, no. 5 (2011): G684—G696. http://dx.doi.org/10.1152/ajpgi.00474.2010.

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The subepithelial intestinal myofibroblast is an important cell orchestrating many diverse functions in the intestine and is involved in growth and repair, tumorigenesis, inflammation, and fibrosis. The myofibroblast is but one of several α-smooth muscle actin-positive (α-SMA+) mesenchymal cells present within the intestinal lamina propria, including vascular pericytes, bone marrow-derived stem cells (mesenchymal stem cells or hematopoietic stem cells), muscularis mucosae, and the lymphatic pericytes (colon) and organized smooth muscle (small intestine) associated with the lymphatic lacteals.

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McElhinney, Kealan, Mustapha Irnaten, and Colm O’Brien. "p53 and Myofibroblast Apoptosis in Organ Fibrosis." International Journal of Molecular Sciences 24, no. 7 (2023): 6737. http://dx.doi.org/10.3390/ijms24076737.

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Organ fibrosis represents a dysregulated, maladaptive wound repair response that results in progressive disruption of normal tissue architecture leading to detrimental deterioration in physiological function, and significant morbidity/mortality. Fibrosis is thought to contribute to nearly 50% of all deaths in the Western world with current treatment modalities effective in slowing disease progression but not effective in restoring organ function or reversing fibrotic changes. When physiological wound repair is complete, myofibroblasts are programmed to undergo cell death and self-clearance, ho

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Bauer, Tyler, Kevin Mangum, Emily Barrett, et al. "TGFb-JMJD3 pathway regulates fibroblast to myofibroblast transition in wound repair." Journal of Immunology 212, no. 1_Supplement (2024): 0790_6658. http://dx.doi.org/10.4049/jimmunol.212.supp.0790.6658.

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Abstract In normal wound healing, resident fibroblasts transition to myofibroblasts, which function to contract and close wounds. In pathologic conditions where wounds fail to heal (such as diabetes), fibroblasts do not increase myofibroblast gene expression; this mechanism is poorly understood. Using human wound scSeq and murine transgenic models, we examined the epigenetic mechanisms that may regulate this transition in the setting of injury. First, we identify that the cytokine TGFb increases myofibroblast genes in vitro. We performed an epigenetic superarray on TGFb-stimulated dermal fibro

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Drobic, Vanja, Ryan H. Cunnington, Kristen M. Bedosky та ін. "Differential and combined effects of cardiotrophin-1 and TGF-β1 on cardiac myofibroblast proliferation and contraction". American Journal of Physiology-Heart and Circulatory Physiology 293, № 2 (2007): H1053—H1064. http://dx.doi.org/10.1152/ajpheart.00935.2006.

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Myofibroblasts respond to an array of signals from mitogens and cytokines during the course of wound healing following a myocardial infarction (MI), and these signals may coordinate ventricular myofibroblast proliferation. Furthermore, myofibroblasts are contractile and contribute to wound contraction by imparting mechanical tension on surrounding extracellular matrix. Although TGF-β1, CT-1, and PDGF-BB participate in various stages of post-MI wound healing, their combined net effect(s) on myofibroblast function is unknown. We investigated myofibroblast proliferation, expression of cell cycle

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Miró, Lluïsa, Anna Pérez-Bosque, Mònica Maijó, Concepció Amat, Richard J. Naftalin, and Miquel Moretó. "Aldosterone induces myofibroblast EGF secretion to regulate epithelial colonic permeability." American Journal of Physiology-Cell Physiology 304, no. 9 (2013): C918—C926. http://dx.doi.org/10.1152/ajpcell.00292.2012.

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In vivo studies show that raised aldosterone (Aldo) during low-Na adaptation regulates the growth of pericryptal myofibroblasts and reduces the permeability of the colonic epithelium. The aim of this study was to reproduce in vitro the in vivo condition of increased Aldo using human CCD-18Co myofibroblasts and T84 colonic epithelial cells to measure myofibroblast and epithelial proliferation and the expression of intercellular junction proteins. Proliferation was quantified by measuring 5-bromo-2′-deoxyuridine incorporation. The myofibroblast expression of EGF, VEGFa, and transforming growth f

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Gabasa, Marta, Paula Duch, Ignasi Jorba, et al. "Epithelial contribution to the profibrotic stiff microenvironment and myofibroblast population in lung fibrosis." Molecular Biology of the Cell 28, no. 26 (2017): 3741–55. http://dx.doi.org/10.1091/mbc.e17-01-0026.

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The contribution of epithelial-to-mesenchymal transition (EMT) to the profibrotic stiff microenvironment and myofibroblast accumulation in pulmonary fibrosis remains unclear. We examined EMT-competent lung epithelial cells and lung fibroblasts from control (fibrosis-free) donors or patients with idiopathic pulmonary fibrosis (IPF), which is a very aggressive fibrotic disorder. Cells were cultured on profibrotic conditions including stiff substrata and TGF-β1, and analyzed in terms of morphology, stiffness, and expression of EMT/myofibroblast markers and fibrillar collagens. All fibroblasts acq

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Doan, K. Tu, Pratiksha Kshetri, Natthapume Attamakulsri, et al. "The Effect of Chitosan Derivatives on the Compaction and Tension Generation of the Fibroblast-populated Collagen Matrix." Molecules 24, no. 15 (2019): 2713. http://dx.doi.org/10.3390/molecules24152713.

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Fibrotic diseases, such as Dupuytren’s contracture (DC), involve excess scar tissue formation. The differentiation of fibroblasts into myofibroblasts is a significant mechanism in DC, as it generates tissue contraction in areas without wound openings, leading to the deposition of scar tissue, and eventually flexing one or more fingers in a restrictive fashion. Additionally, DC has a high recurrence rate. Previously, we showed that N-dihydrogalactochitosan (GC), an immunostimulant, inhibited myofibroblast differentiation in a DC fibroblast culture. Our goal of this study was to expand our previ

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Seymour, Michelle L., David G. Binion, Steven J. Compton, Morley D. Hollenberg, and Wallace K. MacNaughton. "Expression of proteinase-activated receptor 2 on human primary gastrointestinal myofibroblasts and stimulation of prostaglandin synthesis." Canadian Journal of Physiology and Pharmacology 83, no. 7 (2005): 605–16. http://dx.doi.org/10.1139/y05-046.

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It is known that subepithelial myofibroblast-derived prostaglandin (PG)E2 can regulate intestinal epithelial cell functions, and that proteinase-activated receptor-2 (PAR2) is abundantly expressed in the gastrointestinal tract. Since PAR2 activation has previously been associated with stimulation of PGE2 synthesis, we hypothesized that PAR2 expressed on primary human gastrointestinal myofibroblasts regulates PGE2 synthesis via cyclooxygenase (COX)-1 and (or) COX-2, and associated PGE synthases. Primary human myofibroblasts were isolated from the resection tissue of the esophagus, small intesti

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Manetti, Mirko, Eloisa Romano, Irene Rosa, et al. "Systemic Sclerosis Serum Steers the Differentiation of Adipose-Derived Stem Cells Toward Profibrotic Myofibroblasts: Pathophysiologic Implications." Journal of Clinical Medicine 8, no. 8 (2019): 1256. http://dx.doi.org/10.3390/jcm8081256.

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Systemic sclerosis (SSc; scleroderma) is characterized by life-threatening progressive multiorgan fibrosis orchestrated by profibrotic myofibroblasts originating from different sources. Because recent data demonstrated that the majority of myofibroblasts in a murine scleroderma model arise from adipocytic progenitors through the adipocyte-myofibroblast transition process, we sought to determine whether the SSc microenvironment may affect the differentiation potential of adipose-derived stem cells (ADSC). Normal human ADSC from three donors were treated with serum from SSc patients (n = 6), ser

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Michalik, Marta, Katarzyna Wójcik-Pszczoła, Milena Paw, et al. "Fibroblast-to-myofibroblast transition in bronchial asthma." Cellular and Molecular Life Sciences 75, no. 21 (2018): 3943–61. http://dx.doi.org/10.1007/s00018-018-2899-4.

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Abstract Bronchial asthma is a chronic inflammatory disease in which bronchial wall remodelling plays a significant role. This phenomenon is related to enhanced proliferation of airway smooth muscle cells, elevated extracellular matrix protein secretion and an increased number of myofibroblasts. Phenotypic fibroblast-to-myofibroblast transition represents one of the primary mechanisms by which myofibroblasts arise in fibrotic lung tissue. Fibroblast-to-myofibroblast transition requires a combination of several types of factors, the most important of which are divided into humoural and mechanic

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Lecarpentier, Yves. "Mechanical and Thermodynamic Properties of Mesenchymal Stem Cells Differentiated into Myofibroblasts: A Commentary on the Article “Statistical Mechanics of Non-Muscle Myosin IIA in Human Bone Marrow-Derived Mesenchymal Stromal Cells Seeded in a Collagen Scaffold: A Thermodynamic Near-Equilibrium Linear System Modified by the Tripeptide Arg-Gly-Asp (RGD)”." Journal of Stem Cells Research, Development & Therapy 7, no. 3 (2021): 1–4. http://dx.doi.org/10.24966/srdt-2060/100075.

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Mesenchymal Stem Cells (MSCs) are multipotent stromal cells found in bone marrow and have the capacity to differentiate into myofibroblast. In contractile myofibroblasts, the molecular motor is the non-muscle myosin (NMIIA) which differs from the muscle myosin by its ultra-slow kinetics. The differentiation of MSCs into myofibroblasts is promoted by the “Transforming Growth Factor” (TGF-b) which represents a potentially target against tissue fibrosis and cancer.

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Schmidt, Vanessa, Justus Ohmes, Thanh-Diep Ly, et al. "Human Xylosyltransferase I—An Important Linker between Acute Senescence and Fibrogenesis." Biomedicines 11, no. 2 (2023): 460. http://dx.doi.org/10.3390/biomedicines11020460.

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The human xylosyltransferase isoform XT-I catalyzes the initial step in proteoglycan biosynthesis and represents a biomarker of myofibroblast differentiation. Furthermore, XT-I overexpression is associated with fibrosis, whereby a fibrotic process initially develops from a dysregulated wound healing. In a physiologically wound healing process, extracellular matrix-producing myofibroblasts enter acute senescence to protect against fibrosis. The aim of this study was to determine the role of XT-I in acute senescent proto-myofibroblasts. Normal human dermal fibroblasts were seeded in a low cell d

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Wei, Yu-Syuan, Su-Yi Tsai, Shuei-Liong Lin, Yi-Ting Chen, and Pei-Shiue Tsai. "Methylglyoxal-Stimulated Mesothelial Cells Prompted Fibroblast-to-Proto-Myofibroblast Transition." International Journal of Molecular Sciences 26, no. 2 (2025): 813. https://doi.org/10.3390/ijms26020813.

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During long-term peritoneal dialysis, peritoneal fibrosis (PF) often happens and results in ultrafiltration failure, which directly leads to the termination of dialysis. The accumulation of extracellular matrix produced from an increasing number of myofibroblasts was a hallmark characteristic of PF. To date, glucose degradation products (GDPs, i.e., methylglyoxal (MGO)) that appeared during the heating and storage of the dialysate are considered to be key components to initiating PF, but how GDPs lead to the activation of myofibroblast in fibrotic peritoneum has not yet been fully elucidated.

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Squecco, Roberta, Flaminia Chellini, Eglantina Idrizaj та ін. "Platelet-Rich Plasma Modulates Gap Junction Functionality and Connexin 43 and 26 Expression During TGF-β1–Induced Fibroblast to Myofibroblast Transition: Clues for Counteracting Fibrosis". Cells 9, № 5 (2020): 1199. http://dx.doi.org/10.3390/cells9051199.

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Skeletal muscle repair/regeneration may benefit by Platelet-Rich Plasma (PRP) treatment owing to PRP pro-myogenic and anti-fibrotic effects. However, PRP anti-fibrotic action remains controversial. Here, we extended our previous researches on the inhibitory effects of PRP on in vitro transforming growth factor (TGF)-β1-induced differentiation of fibroblasts into myofibroblasts, the effector cells of fibrosis, focusing on gap junction (GJ) intercellular communication. The myofibroblastic phenotype was evaluated by cell shape analysis, confocal fluorescence microscopy and Western blotting analys

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Dobie, Ross, and Neil C. Henderson. "Homing in on the hepatic scar: recent advances in cell-specific targeting of liver fibrosis." F1000Research 5 (July 19, 2016): 1749. http://dx.doi.org/10.12688/f1000research.8822.1.

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Despite the high prevalence of liver disease globally, there are currently no approved anti-fibrotic therapies to treat patients with liver fibrosis. A major goal in anti-fibrotic therapy is the development of drug delivery systems that allow direct targeting of the major pro-scarring cell populations within the liver (hepatic myofibroblasts) whilst not perturbing the homeostatic functions of other mesenchymal cell types present within both the liver and other organ systems. In this review we will outline some of the recent advances in our understanding of myofibroblast biology, discussing bot

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Xu, Keli, Erica Nieuwenhuis, Brenda L. Cohen, et al. "Lunatic Fringe-mediated Notch signaling is required for lung alveogenesis." American Journal of Physiology-Lung Cellular and Molecular Physiology 298, no. 1 (2010): L45—L56. http://dx.doi.org/10.1152/ajplung.90550.2008.

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Distal lung development occurs through coordinated induction of myofibroblasts, epithelial cells, and capillaries. Lunatic Fringe ( Lfng) is a β1–3 N-acetylglucosamine transferase that modifies Notch receptors to facilitate their activation by Delta-like (Dll1/4) ligands. Lfng is expressed in the distal lung during saccular development, and deletion of this gene impairs myofibroblast differentiation and alveogenesis in this context. A similar defect was observed in Notch2 β-geo/+ Notch3 β-geo/β-geo compound mutant mice but not in Notch2 β-geo/+ or Notch3 β-geo/β-geo single mutants. Finally, to

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Evanko, Stephen P., Michel D. Gooden, Inkyung Kang, Christina K. Chan, Robert B. Vernon, and Thomas N. Wight. "A Role for HAPLN1 During Phenotypic Modulation of Human Lung Fibroblasts In Vitro." Journal of Histochemistry & Cytochemistry 68, no. 11 (2020): 797–811. http://dx.doi.org/10.1369/0022155420966663.

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Hyaluronan and proteoglycan link protein 1 (HAPLN1) stabilizes interactions between two important extracellular matrix (ECM) macromolecules, versican and hyaluronan, which facilitate proliferation of fibroblasts and their conversion to myofibroblasts. However, the role of HAPLN1 in these events has not been studied. Using immunocytochemistry, cellular and ECM locations of HAPLN1 were evaluated in cultured human lung fibroblasts during proliferation and conversion to myofibroblasts. HAPLN1 localized to pericellular matrices, associating with both versican and hyaluronan in the ECM and on the ce

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Cai, Guo-Qiang, Chu-Fang Chou, Meng Hu та ін. "Neuronal Wiskott-Aldrich syndrome protein (N-WASP) is critical for formation of α-smooth muscle actin filaments during myofibroblast differentiation". American Journal of Physiology-Lung Cellular and Molecular Physiology 303, № 8 (2012): L692—L702. http://dx.doi.org/10.1152/ajplung.00390.2011.

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Myofibroblasts are implicated in pathological stromal responses associated with lung fibrosis. One prominent phenotypic marker of fully differentiated myofibroblasts is the polymerized, thick cytoplasmic filaments containing newly synthesized α-smooth muscle actin (α-SMA). These α-SMA-containing cytoplasmic filaments are important for myofibroblast contractility during tissue remodeling. However, the molecular mechanisms regulating the formation and maturation of α-SMA-containing filaments have not been defined. This study demonstrates a critical role for neuronal Wiskott-Aldrich syndrome prot

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Younesi, Fereshteh Sadat, and Boris Hinz. "The Myofibroblast Fate of Therapeutic Mesenchymal Stromal Cells: Regeneration, Repair, or Despair?" International Journal of Molecular Sciences 25, no. 16 (2024): 8712. http://dx.doi.org/10.3390/ijms25168712.

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Mesenchymal stromal cells (MSCs) can be isolated from various tissues of healthy or patient donors to be retransplanted in cell therapies. Because the number of MSCs obtained from biopsies is typically too low for direct clinical application, MSC expansion in cell culture is required. However, ex vivo amplification often reduces the desired MSC regenerative potential and enhances undesired traits, such as activation into fibrogenic myofibroblasts. Transiently activated myofibroblasts restore tissue integrity after organ injury by producing and contracting extracellular matrix into scar tissue.

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Grove, Lisa M., Maradumane L. Mohan, Susamma Abraham та ін. "Translocation of TRPV4-PI3Kγ complexes to the plasma membrane drives myofibroblast transdifferentiation". Science Signaling 12, № 607 (2019): eaau1533. http://dx.doi.org/10.1126/scisignal.aau1533.

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Myofibroblasts are key contributors to pathological fibrotic conditions of several major organs. The transdifferentiation of fibroblasts into myofibroblasts requires both a mechanical signal and transforming growth factor–β (TGF-β) signaling. The cation channel transient receptor potential vanilloid 4 (TRPV4) is a critical mediator of myofibroblast transdifferentiation and in vivo fibrosis through its mechanosensitivity to extracellular matrix stiffness. Here, we showed that TRPV4 promoted the transdifferentiation of human and mouse lung fibroblasts through its interaction with phosphoinositid

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