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PubMed2004

Inflammatory myofibroblastic tumor presenting as a pancreatic mass: a case report and review of the literature.

CONTEXT: Inflammatory myofibroblastic tumor is a distinctive lesion of unknown etiology. It has generally been considered a rare benign pseudosarcomatous lesion of admixed inflammatory infiltrates with myofibroblastic spindle cells. Although original case descriptions focused on the pulmonary system, it is now recognized that virtually any anatomic location can be involved. However, an inflammatory myofibroblastic tumor located in the pancreas is rare. CASE REPORT: We report a case of an asymptomatic 70-year-old Caucasian man with a 3.8 cm inflammatory myofibroblastic tumor located in the tail of the pancreas which was discovered incidentally on a computed tomography scan of the abdomen. Endoscopic ultrasonography with fine needle aspiration was negative for malignancy. However, because of worrisome radiographic features, a distal pancreatectomy with splenectomy was performed. The pathology revealed an inflammatory myofibroblastic tumor with focal extension into the peripancreatic soft tissues, but with negative surgical margins. The patient has been followed for 10 months without evidence of recurrence. CONCLUSIONS: To date, there have been only 25 cases of inflammatory myofibroblastic tumor located in the pancreas reported in the English language scientific literature. Even with multimodal pre-surgical investigation, it can be extremely difficult to differentiate inflammatory myofibroblastic tumor from pancreatic malignancies. Most cases require surgical exploration and complete resection to obtain an accurate diagnosis. A review of published case reports is also presented.

Aged↗

PubMed2005

[Connective tissue growth factor promotes the proliferation of myofibroblast through Erk-1/2 signaling pathway].

OBJECTIVE: To investigate the mechanism by which connective tissue growth factor (CTGF) enhances transforming growth factor-beta(1) (TGF-beta(1))-mediated myofibroblastic activation in renal interstitial fibroblast NRK-49F. METHODS: NRK-49F cells were pretreated by TGF-beta(1) so that some cells transform into myofibroblasts, and then the cells were devided into vechile, CTGF treated group, TGF-beta(1) treated group, and PD98059 intervene group. The hallmark of myofibroblast, alpha-SMA immunostaining and marker of cellular proliferation, BrdU incorporation were determined by immunocytochemistry doublestaining. The protein level of alpha-SMA was determined by Western blot analysis. RESULTS: CTGF induced a proliferative response in myofibroblast initiated by TGF-beta(1), whereas TGF-beta(1) had no action on proliferation. Although CTGF could not induce myofibroblastic activation in renal interstitial fibroblast, it upregulated the protein level of alpha-smooth muscle actin significantly in cells pretreated by TGF-beta1 (P < 0.05). Significant phosphorylation of Erk-1/2 was detected after incubation with CTGF for 30 min in the cells pretreated by TGF-beta(1), while TGF-beta(1) did not have this ability. Inhibition of Erk-1/2 activation by Mek kinase inhibitor PD98059 suppressed CTGF-mediated myofibroblasts proliferation and significantly down-regulated expression of alpha-SMA protein in cells pretreated by TGF-beta(1) (P < 0.05). CONCLUSION: CTGF induced a proliferative response in TGF-beta(1)-initiated myofibroblasts, and this action is likely dependent on the activation of Erk-1/2 signaling pathway.

Animals↗

PubMed2006

Stromal myofibroblasts in breast cancer: relations between their occurrence, tumor grade and expression of some tumour markers.

It is suggested that tumour stromal myofibroblasts exert an unfavourable effect on the biology of breast cancer. We are aware of only a single study which examined relationships between manifestation of myofibroblasts in the stroma of breast cancer and clinicopathological data of the patients. The present study was aimed at estimation of the effect exerted by myofibroblasts present in the tumour stroma on principal pathological parameters and on expression of Ki67, P53 and HER-2 proteins in the group of the most frequent breast cancers, the ductal cancers. In paraffin sections of 60 ductal breast cancers (20 cases in G1, 20 in G2 and 20 in G3), immunohistochemical reactions were performed to detect expression of smooth muscle actin (SMA) in order to visualize myofibroblasts, Ki67, P53 and HER-2. The studies demonstrated that the most numerous myofibroblasts were present in G3 cases and they were the least frequent in G1 cases (P = 0.02). Positive correlations were observed between the presence of myofibroblasts in tumour stroma and expression of Ki67 and HER-2 in breast cancer cells in the entire group (P < 0.001 and P = 0.001, respectively), in G2 cases (P = 0.003 and P = 0.03) and in G3 cases (P = 0.01 and P = 0.03). Considering that the higher grade, Ki67 and HER-2 are thought to represent unfavourable prognostic factors, the elevated content of myofibroblasts in tumour stroma is probably typical for cases with worse prognosis.

Actins↗

PubMed1995

[Roles of myofibroblasts in the stroma of human gastric carcinoma].

The stromal reaction of human gastric carcinoma was studied about myofibroblast proliferation and collagen type I, III synthesis in 28 surgical materials (15 cases of well differentiated type, 13 cases of poorly differentiated type), using immunohistochemical and immunoelectron microscopical techniques. Immunohistochemically, myofibroblasts showed marked reactivity to both anti-alpha smooth muscle actin (alpha SM-1) MAb and anti-vimentin MAb, and they were broadly distributed in the stroma of gastric carcinomas. Moreover, myofibroblasts revealed their own characteristics surrounding collagenous fibers under electron microscope. The myofibroblast proliferation was more prominent in poorly differentiated carcinoma and invasive carcinomas. On the other hand, much more myofibroblasts were observed in the marginal portion of cancer nests than the central area. The distribution of collagen type III was very similar to that of myofibroblast. These findings suggest that the proliferation of myofibroblast and collagen synthesis in tumor stroma were obvious host response against carcinomas, and this phenomenon may reveal an important biological status in gastric carcinoma.

Adenocarcinoma↗

PubMed1998

Functional gap junctions in corneal fibroblasts and myofibroblasts.

PURPOSE: Within the corneal stroma, keratocytes communicate through gap junctions. These plasma membrane channels, which connect the cytoplasm of adjacent cells, are composed of connexins. In a cell culture model, an investigation was conducted to determine whether connexin-based gap junction intercellular communication is present in fibroblasts and myofibroblasts, both of which replace keratocytes after wounding. METHODS: Fibroblasts and myofibroblasts were grown according to preestablished methods. Phenotype was determined by immunocytochemistry. A gap junction-permeant dye, Lucifer yellow or Cascade blue, and nonpermeant 10-kDa Texas red-dextran were used. Tracer fluorescent dyes were introduced by scrape-loading or by microinjection, and their diffusion into adjacent cells was recorded photographically. Inhibition of gap junction dye transfer was elicited by treatment with 18-alpha-glycyrrhetinic acid (AGA). RESULTS: In confluent fibroblast or myofibroblast cultures, the scrape-loaded dextran probe remained within wounded cells, whereas the Lucifer yellow or Cascade blue dye diffused into adjacent intact cells. Similarly, in nonconfluent fibroblast and myofibroblast cultures, microinjected Lucifer yellow rapidly diffused from the microinjected cell to adjacent cells. Treatment with 2 microM AGA, an uncoupling agent, blocked the spread of Lucifer yellow in fibroblast and myofibroblast cultures. CONCLUSIONS: Cultured fibroblasts and myofibroblasts have functional gap junctions as has previously been demonstrated for keratocytes in vivo. Thus, fibroblasts and myofibroblasts have the ability to establish and maintain intercellular communication with themselves and with nonactivated keratocytes. This property may be critical in the wound-healing process, especially in the avascular corneal environment.

Actins↗

PubMed2000

The effect of environmental cues on the differentiation of myofibroblasts in peritoneal granulation tissue.

This study investigated the effect of haemodynamic stress, active stretch, and neuronal input on the differentiation of myofibroblasts in peritoneal granulation tissue. Lengths of silastic tubing (10 mm long x 3 mm diameter) were placed in the peritoneal cavity of the rat. By 2 weeks, a capsule of granulation tissue had formed around the tubing. This capsule consisted of several layers of myofibroblasts and the matrix that they had produced, overlaid by a single layer of mesothelial cells. The silastic tubing was removed and at the same time, the living tube of tissue was everted so that the mesothelium now lined its inner surface. To examine the effect of haemodynamic factors on myofibroblast differentiation, the 10 mm long tubes of mesothelial-lined granulation tissue were transplanted into the severed abdominal aorta of the same rat in which the granulation tissue was grown. End-to-end anastomoses were performed to extend the existing aorta. At 1, 2, and 3 months post-transplantation, the grafts were removed and a progressive increase in the percent volume fraction of myofilaments (% V(v)myo) was observed (from 35.7+/-1.6% to 58.7 3+/-1.4%; p<0.05). To determine whether the active stretching that occurs in vivo could account for differentiation of the constituent myofibroblasts, tubes of granulation tissue were placed into a mechanical device in which they underwent continuous stretching of 5-10% elongation from the resting position at 50 cycles per minute for 3, 24 or 72 h. This caused a significant (p<0. 05) increase in %V(v)myo after 72 h. Granulation tissue was also transplanted into the rat anterior eye chamber, where it became surrounded by adrenergic nerves supplying the host iris. Two months after implantation, there was no significant change in the %V(v)myo of the myofibroblasts (35.7+/-1.6% to 33.3+/-2.7%). These studies show that myofibroblasts of the granulation tissue encapsulating free-floating foreign bodies in the peritoneal cavity further differentiate towards a smooth muscle phenotype when transplanted into a smooth muscle environment, namely the abdominal aorta. Similar changes are seen when the granulation tissue is subjected to active, intermittent stretch in vitro, while the presence of nerves has no effect.

Animals↗

PubMed2006

Myofibroblasts and hyalinized collagen as markers of skin disease in systemic sclerosis.

OBJECTIVE: To investigate the correlation between the degree of dermal fibrosis and myofibroblast infiltration using clinical assessments of skin thickness and hardness in systemic sclerosis (SSc). METHODS: Eleven patients with diffuse SSc and 10 healthy controls were evaluated using the modified Rodnan skin thickness score and durometry (hardness measurement). Biopsy samples were obtained from the dorsal mid-forearm in all subjects at the baseline visit and again 6-12 months later in patients with SSc. Five of the patients with SSc received treatment with cyclophosphamide (CYC) in the interval between skin biopsies. Biopsy sections were assessed for myofibroblast and hyalinized collagen content by 2 blinded observers. RESULTS: Myofibroblast and hyalinized collagen scores each correlated with the forearm skin score (r = 0.83, P < 0.0001 and r = 0.78, P < 0.0001, respectively) and with the forearm durometry score (r = 0.72, P < 0.0004 and r = 0.69, P < 0.0008, respectively). The change in the dermal hyalinized collagen score correlated with the change in the forearm durometry score (r = 0.74, P < 0.0213). The myofibroblast score decreased in all 5 patients who received CYC and increased in those receiving non-CYC treatments (P < 0.01 for the difference). CONCLUSION: Myofibroblasts play an important role in the pathogenesis of fibrosis, and our data imply that quantification of myofibroblasts and hyalinized collagen in skin may be a useful outcome measure in clinical studies of SSc.

Adult↗

PubMed1994

In vivo and in vitro invasiveness of a rat colon-cancer cell line maintaining E-cadherin expression: an enhancing role of tumor-associated myofibroblasts.

In various cell systems, an inverse relationship was found between expression of E-cadherin, a molecule involved in the Ca(2+)-dependent homophylic cell-to-cell attachment of epithelial cells, and the capacity to invade extracellular matrix gels or normal tissues in vitro. DHD/K12/TRb (PROb) cells, maintained as a cell line derived from a rat colon carcinoma, homogeneously expressed in vitro immunoreactive E-cadherin, which was functional as shown in cell dissociation-reassociation assays. PROb cells were found to be non-invasive in 3 different assays in vitro. However, tumors resulting from a s.c. injection of PROb cells into syngeneic BD-IX rats were invasive, although PROb cells maintained E-cadherin expression in the tumors. Cells from a freshly dissociated PROb tumor showed, not only PROb cells but also tumor-associated myofibroblasts and were able to cross a Matrigel-coated filter. PROb tumors were indeed infiltrated by numerous myofibroblasts, mainly located at the invasive edge of the tumor. Cells from an established culture of tumor-infiltrating myofibroblasts were able to confer upon PROb cells invasiveness through Matrigel-coated filter or into chick-heart fragments. PROb cells maintained their capacity to express E-cadherin after myofibroblast-enhanced Matrigel invasion. Tumor-associated myofibroblasts, but not PROb cells, secreted a 72-kDa collagenase that could play a role in tumor-cell invasion. These results strongly suggest that cells from the tumor stroma, and more specifically myofibroblasts, may be involved in the invasiveness of epithelial tumor cells in vivo, even when E-cadherin expression prevents tumor-cell invasiveness in different in vitro assays.

Animals↗

PubMed2004

Normal skin wound and hypertrophic scar myofibroblasts have differential responses to apoptotic inductors.

During wound healing, myofibroblasts play a central role in matrix formation and wound contraction. At the end of healing, there is evidence that myofibroblasts disappear via apoptotic pathways. Hypertrophic scars are a fibroproliferative disorder that leads to considerable morbidity. It has been postulated that a defect in myofibroblast apoptosis could be responsible for the pathological scar formation, but no evidence exists. We have isolated and cultured human normal wound (Wmyo) and hypertrophic scar (Hmyo) myofibroblasts and compared their basal apoptotic rates and their sensitivity to serum starvation and Fas antibody-induced apoptosis to that obtained for dermal fibroblasts (Fb). A higher rate of apoptosis as evidenced by morphological criteria and a propidium iodide assay was observed for Wmyo in comparison to Fb and Hmyo. These results came along with a low level of the anti-apoptotic proteins Bcl-2 and Bclx(L) in Wmyo, whereas there was an increase in the level of the pro-apoptotic molecule Bax when compared to the results obtained for Fb and Hmyo. Hmyo showed a higher level of Bcl-2 compared to Fb but no difference in the Bax or Bclx(L) level. After serum starvation, Wmyo revealed an increased apoptotic rate, whereas Hmyo and Fb did not show any difference. Anti-Fas treatment did not modify the levels of apoptosis but strongly increased the cell growth of Hmyo as compared to Wmyo. This is the first study presenting a broad vision of the apoptotic sensitivity of normal and pathological myofibroblasts. These results confirmed the hypothesis of defects in apoptosis and growth during pathological scar formation impeding myofibroblast disappearance at the end of healing.

Actins↗

PubMed1992

The peritubular myofibroblasts in the testes from normal men and men with Klinefelter's syndrome. A quantitative, ultrastructural, and immunohistochemical study.

The ultrastructure and immunostaining with antibodies against actin, desmin, and vimentin were studied in the peritubular myofibroblasts of testes from normal men and men with Klinefelter' syndrome (KS). The seminiferous tubules were classified into five types (a-e), related to the progressive degree of sclerosis measured as thickening of the lamina propria. In control testes, only types a and b tubules were present, whereas the testes from men with KS showed types b, c, d, and e tubules. The ultrastructural study revealed abundant microfilament bundles with electron-dense bodies in the cell periphery of the myofibroblasts in a and b tubules. In c tubules, the microfilament bundles of the myofibroblasts were lacking in electron-dense bodies. Myofibroblasts in tubules d and e showed scanty microfilament bundles. Immunostaining of peritubular myofibroblasts with anti-actin antibodies was intense in tubule types a-c and scanty in types d and e. Immunostaining of myofibroblasts with anti-desmin antibodies was intense in tubule types a and b, and negative in types c-e. Immunostaining with anti-vimentin antibodies was weak in tubule types a-c and intense in types d and e. Quantitative study revealed that with the progression of sclerosis, the number and volume per cross-sectioned tubule of actin-containing cells and, mainly, desmin-containing cells decrease while the number and volume of vimentin-containing cells increase.

Actins↗

PubMed2001

Nongenomic estrogen action in human lung myofibroblasts.

Recent studies have suggested that the antiproliferative effects of E2 may be mediated through a nongenomic action. Herein, we asked whether nongenomic estrogen action regulates phosphorylation of Raf1 and ERK1/2 mitogen-activated protein (MAP) kinase in lung myofibroblasts. We demonstrated that lung myofibroblasts, incubated in the presence of E2, showed a rapid phosphorylation on serine-259 of Raf1 and tyrosine-204 of ERK1/2 MAP kinase at 15 min, by approximately 3- and 5-fold, respectively. This phosphorylation was followed by dephosphorylation between 30 and 60 min. Western blot analysis showed that E2 regulates tyrosine phosphorylation of four main cytoplasmic proteins in lung myofibroblasts, of 42, 44, 70 and 100 kDa. Furthermore, our results indicated that E2 inhibits cell proliferation (BrdU index) in lung myofibroblasts by approximately 30% (P < 0.01). These data provide evidence that nongenomic action of E2, regulates both serine and tyrosine phosphorylation of cytoplasmic proteins in lung myofibroblasts, including Raf1 and ERK1/2 MAP kinase, which may regulate proliferation in lung myofibroblasts.

Binding Sites↗

PubMed1995

Factors influencing myofibroblast differentiation during wound healing and fibrosis.

Granulation tissue fibroblasts (myofibroblasts) develop several ultrastructural and biochemical features of smooth muscle (SM) cells, including the presence of microfilaments bundles and the expression of alpha-SM actin, the actin isoform typical of contractile vascular SM cells. Myofibroblasts have been suggested to play a role in wound contraction and in retractile phenomena observed during fibrotic diseases. When granulation tissue evolves into a scar, myofibroblasts containing alpha-SM actin disappear, probably as a result of apoptosis. In contrast myofibroblasts expressing alpha-Sm actin persist in excessive scarring and in fibrotic conditions. The mechanisms leading to the development of myofibroblastic features remain to be investigated. Studies on the factors regulating the phenotype of myofibroblasts will be necessary for understanding their behavior in vivo, and possibly modifying this behavior during the different clinical settings.

Animals↗

PubMed1981

The effect of stretching on formation of myofibroblasts in mouse skin.

Wound contraction results from the contractile activity of modified fibroblasts, termed myofibroblasts, which are present in the granulation tissue of the healing wound. This study examines the relative role of mechanical tension (stretching) and wound healing as events capable of stimulating the formation of myofibroblasts in mouse skin. The skin of hairless mice was subjected to mechanical stretching and to a small incisional wound either separately or in combination. Animals were killed at intervals between 1 and 6 days and the dermis examined with the electron microscope. Stretching alone produced little evidence of inflammation at any time interval but cells with the ultrastructural characteristics of myofibroblasts were present at 4 days and abundant at 6 days. Skin that had been both stretched and wounded showed a marked inflammatory response and also contained myofibroblasts, but they were less frequent than in the skin subjected to stretching alone. Very few myofibroblasts were evident in skin that had only been wounded. It is suggested that the effect of mechanical tension alone may initiate formation of myofibroblasts in a tissue.

Animals↗

PubMed1981

Stromal myofibroblasts in primary invasive and metastatic carcinomas. A combined immunological, light and electron microscopic study.

A series of 23 primary invasive and 7 metastatic carcinomas was examined by light microscopy (LM), transmission electron microscopy (TEM) and immunofluorescence (IF), the latter employing an anti-actin antibody. The results were correlated with macroscopic features such as retraction and consistency. Stromal cells rich in actin, readily identified by IF in firm and retracted carcinomas, were rare or absent in neoplasms lacking these features. TEM established the myofibroblastic nature of these stromal cells. Alternate sections (LM, IF) of each neoplasm demonstrated that myofibroblasts were more numerous in "young" mesenchymal stroma than in densely sclerotic areas. The connective tissue adjacent to intraductal mammary carcinoma lacked myofibroblasts, suggesting that epithelial stromal invasion is required to evoke a myofibroblastic stromal response. Myofibroblasts which possess synthetic (type III collagen) and contractile properties may well contribute to the firm consistency and retraction which characterize many carcinomas. The induction of myofibroblasts might represent an important host stromal response directed toward containment of invasive and/or metastatic carcinoma. This response may be especially important in neoplasms with weak antigenicity and/or slow doubling times.

Actins↗

PubMed2000

Myofibroblasts in adolescent varicocele: an ultrastructural and immunohistochemical study.

Myofibroblasts of the testes play an important role in the morphofunctional integrity of the seminiferous tubule. Previous studies in adults with varicocele have demonstrated an involvement of this cell population that tends to transform into fibroblasts. The aim of the present study was to try and verify the morphological features of myofibroblasts in the adolescent with left idiophatic varicocele. Twenty-two testicular biopsies were obtained from adolescents (aged 13-18 years, mean 15.8) and operated for left idiophatic varicocele. Biopsies were processed for electron microscopy (TEM) and immunofluorescence studies. The latter determined the level of myofibroblasts by using alpha-smooth muscle isoactin, a specific marker of myofibroblasts and, hence, excluding fibroblasts. TEM observations revealed a normal ultrastructure of myofibroblasts that was similar to that for the controls but an increased presence of extracellular matrix. The immunofluorescence study always demonstrated strong cell positivity to anti alpha-smooth muscle isoactin as also seen in the controls. This study demonstrates that adolescents with varicocele have well preserved myofibroblasts and do not show any evidence of transformation into fibroblasts, this has already been demonstrated in adult varicocele. These observations could represent an important factor for the understanding of the reversal of growth failure of the testes observed after early treatment.

Adolescent↗

PubMed1998

[Myofibroblastic tumors. Brief review of clinical aspects, diagnosis and differential diagnosis].

This review summarizes myofibroblastic tumours that have been characterized in the last years. These lesions include: fibromatoses in adults and infants (infantile digital fibromatosis and infantile myofibromatosis); myofibroma of adults, an almost exclusively solitary lesion in the skin which is characterized morphologically as a biphasic lesion composed of spindle-shaped eosinophilic tumour cells and more primitive mesenchymal tumour cells associated with a haemangiopericytoma-like vasculature; dermatomyofibroma (plaque-like dermal fibromatosis), a band-like myofibroblastic proliferation in young female patients, which is mainly located in the periaxillar region and in which distinction from more aggressive, plaque-like variant of dermatofibrosarcoma protuberans is mandatory; myofibroblastoma of the breast, a well-circumscribed lesion composed of spindle shaped, desmin-positive tumour cells, which is seen mainly in elderly male patients and has to be distinguished from other spindle cell lesions of the breast; angiomyofibroblastoma, a well-circumscribed myofibroblastic neoplasm of the vulva and vagina composed of avoid to round myoid tumour cells with scattered multinucleated cells, which forms a continuous morphological spectrum with the clinically more aggressive angiomyxoma in this location; intranodal myofibroblastoma, a distinctive proliferation of myofibroblastic cells associated with so-called amianthoid fibres, which is seen most commonly in inguinal lymph nodes; myofibroblastoma/myofibroblastic tumour of soft tissues, a variably well-circumscribed myofibroblastic lesion which lacks atypia and is composed of actin and/or desmin positive tumour cells, and poorly delineated sarcomas with myofibroblastic differentiation (myofibrosarcoma).

Adult↗

PubMed1998

[Myofibroblasts. Review out outlook].

When studying inflammation and wound healing, peculiar fibroblasts with ultrastructural similarities to smooth muscle cells were described by a group of pathologists associated with Guido Majno (GM) and Giulio Gabbiani (GG), subsequently called myofibroblasts. Similar cells were also found later in human granulation tissue, palmar fibromatosis and in stromal reactions with invasive cancers. Their identification was facilitated by immunohistochemical methods. Some neoplastic cells, for instance in MFH, also revealed characteristics compatible with myofibroblasts. Myofibroblasts are conceived of as modulated fibroblasts. Cytokines may serve as mediators for activation and contractile modification of fibroblasts. In this context monitoring of a tumor-like overproduction of myofibroblasts or an underproduction with non-union of wounds might also be feasible. Moreover, better understanding of the role of myofibroblasts concerning the transition from in situ carcinomas into invasive growth may have therapeutic perspectives. Myofibroblasts apparently not only show a temporary existence in disease, but also can be found under normal conditions in several regions, such as the skin, periodontal ligaments, or pulmonary septa.

Cell Transformation, Neoplastic↗

PubMed1988

The fibroblast-like nature of myofibroblasts.

The myofibroblast is found in normal tissue as well as in a wide variety of pathological processes. We have cultured myofibroblasts and dermal fibroblasts and have found that they secrete similar type-specific procollagens into the culture media. These were primarily type I and III procollagens with a predominance of type I procollagen. These patterns are distinctly different from those of smooth muscle cells, which synthesize predominantly type III procollagen. Cultured fixed cells were also examined by immunohistochemistry. Both myofibroblasts and fibroblasts stained positively with antibodies to type I and III procollagens. Reaction to type V procollagen antibodies was prominent only in the myofibroblast, as was immunostaining with anti-muscle actin antibodies. Immunostaining with desmin antibodies was negative in both cell types. By electron microscopy, the myofibroblast had well-developed dense microfilament fibers of 40-80 degrees that were prominent in the long axes of the cells near the cellular margins. Although the myofibroblast has properties of both smooth muscle cells and fibroblasts, it appears to be most likely a modified fibroblast that has undergone differentiation, probably in response to specific signals from the extracellular matrix.

Actins↗