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At least 487 records · Page 27Linked to original sources
PubMed2026

COMMD9-regulated endothelial cell abnormality-induced hypercoagulability is associated with Budd-Chiari syndrome.

BACKGROUND: Budd-Chiari syndrome (BCS) presents diagnostic and treatment challenges owing to its insidious onset. Genetic variants associated with BCS vary geographically; in Asian populations, the condition is primarily caused by membranous obstruction composed of endothelial cells (ECs). A better understanding of the genetic pathogenesis of membranous BCS may offer new insights into disease mechanisms. METHODS: This study employed whole-exome sequencing to identify candidate genes responsible for EC abnormalities in 485 patients with membranous BCS and 329 patients with vascular malformations (VaMs). Functional investigations were conducted to validate the selected genes in vitro and in vivo. RESULTS: Whole-exome data revealed that the frequency of variants in the vascular function-related KLHDC2 exceeded that of JAK2 in BCS. Knockdown of KLHDC2 promoted adhesion and suppressed proliferation of ECs. In addition, 92 genes enriched for rare variants overlapped between BCS and VaMs. Systems biology analysis revealed two gene clusters, including COMMD9, enriched in proteins intolerant to loss-of-function mutations. Furthermore, suppression of COMMD9 impaired EC migration and tube formation, inhibited subintestinal angiogenic sprouting in zebrafish, and elevated EC adhesion. Transcriptomic analysis linked COMMD9 to EC abnormalities via the PI3K-Akt pathway. Commd9 knockdown promoted venous hypercoagulability in vivo following drug or ligation-induced stenosis. CONCLUSIONS: These findings indicate that multiple rare genetic variants, particularly in COMMD9, are involved in the development of membranous BCS by regulating hypercoagulability induced by EC abnormalities. These findings may help guide future clinical research towards improved understanding and treatment of BCS.

Budd–Chiari syndrome↗
PubMed1990

Cholecystokinin, secretin, pancreatic polypeptide in relation to gallbladder dynamics and gastrointestinal interdigestive motility.

Using a combined technique of hepatobiliary scintigraphy and gastrointestinal motility recordings, the changes in blood concentrations of cholecystokinin (CCK), secretin and pancreatic polypeptide (PP) were studied in relation to gastrointestinal motility and gallbladder dynamics in the interdigestive state in 7 healthy male volunteers. No changes in CCK concentration were found in relation to the migrating motor complex (MMC). In 3 subjects a slightly but insignificant elevated secretin level was seen during phase I of the MMC, otherwise no changes were observed. More pronounced fluctuations in PP appeared with significantly higher values during phase III compared to phase II. Values of concentrations of CCK, secretin and PP in periods with gallbladder filling were not significantly different from the values in periods of emptying.

Adult↗
PubMed2003

TLR4 signaling induces TLR2 expression in endothelial cells via neutrophil NADPH oxidase.

Interactions of polymorphonuclear neutrophils (PMNs) with endothelial cells may contribute to the activation of endothelial cell responses involved in innate immunity. We explored a novel function of PMN NADPH oxidase in the mechanism of Toll-like receptor-2 (TLR2) upregulation induced by LPS-TLR4 signaling in endothelial cells. We showed that LPS induced TLR2 up-regulation through TLR4- and MyD88-dependent signaling. In neutropenic mice, the LPS-induced NF-kB activation and TLR2 expression were significantly reduced, and both responses were restored upon repletion by PMN obtained from WT mice but not by PMNs from NADPH oxidase gp91pho(-/-) mice. These findings were recapitulated in mouse lung vascular endothelial cells cocultured with PMNs, indicating that the augmented NF-kB activation and the resultant TLR2 upregulation in endothelial cells were secondary to oxidant signaling generated by PMN NADPH oxidase. The functional relevance of NADPH oxidase in mediating TLR4-induced TLR2 expression in endothelial cells was evident by markedly elevated and stable ICAM-1 expression as well as augmented PMN migration in response to sequential challenge with LPS and peptidoglycan. Thus, PMN NADPH oxidase-derived oxidant signaling is an important determinant of the cross talk between TLR4 and TLR2 and the control of endothelial cell activation.

Animals↗
PubMed1993

[Changes in transaminase before and after tonsillectomy].

Almost all patients who undergo palatine tonsillectomy for chronic tonsillitis and/or tonsillar hypertrophy manifest postoperative changes in their condition and laboratory data. In some patients, high preoperative transaminase levels decrease postoperatively. I studied 17 patients who had abnormal serum transaminase levels 10 days before tonsillectomy. Before tonsillectomy, serum glutamate oxaloacetate transaminase (GOT) levels were abnormal in half and serum glutamate pyruvate transaminase (GPT) were abnormal in all. Before operation, laboratory values of serum GPT were higher than those of serum GOT in all 17 patients. After tonsillectomy, the abnormal GOT levels in all patients gradually improved to the normal range before the 11th postoperative day and GPT levels did so before the 25th day. Measurement of intracellular transaminase activity of the palatine tonsil suggested that the migration of intracellular transaminase from tonsillar cells to serum would not elevate the serum transaminase level. Postoperative changes in serum transaminase and serum cholinesterase were different from the recovery process observed in fatty liver. The high transaminase level observed in patients with tonsillectomy is suspected to be due to other organs, rather than continuous inflammation of the palatine tonsil.

Adult↗
PubMed2000

[The cell as a gravity-dependent biomechanic system].

In the period of 1995-1997 experimental and theoretical studies with various biomechanic objects, i.e. individual cells and cell associations, were performed under changed gravity (0.00001-5 g). Experimental investigations were conducted using clinostats and centrifuges to model effects of hypo- and hypergravity, and aboard space vehicles in real microgravity. Cell cultures in vitro including fibroblasts and osteoblasts on a solid glass or plastic substrate served as objects of the studies. Changes in value and direction of the gravity vector were found to modify the morphophysiological characteristics of cells: structural organization (spatial rearrangement of the intracell component, changes in forms, sizes and quantity of cells) and functional activity (alterations in energy expenditure and intensity of intracellular metabolism). The data suggest that there should be mechanisms of gravitational sensitivity in living systems on the cellular level. As was stated, sensitivity of unicellular free-living organisms to gravity is mostly defined by the motor activity determined by the level of general metabolism. Morphological characteristics (form, size and mass) are of secondary importance. Theoretical analysis resulted in correction of one of the principle postulates of gravitational biology stating a direct link between size (mass) and gravitational sensitivity of organism. Described were consistent patterns of growth, development, and behavior of unicellular cultures in gravitational fields. Strengthening of the force of gravity (hypergravity) leads to eventual deceleration of cell growth and diminution of biomass gain. On the other hand, the spaceflight environment (microgravity) stimulates growth mechanisms. In our opinion, behind these gravitational effects are altered levels of energy spent by cells to overcome the force of gravity. Opposite trends were observed in experiments with cell cultures in vitro. During space microgravity, fibroblast cultures on the solid substrate decreased the growth rate, and inhibited cell division and migration within the substrate. Compared to the Earth's gravity, under elevated gravity these parameters were noticeably higher. It was demonstrated that the main cause of the unfavorable effects of space microgravity on the cellular level is decay in the adherence of cells to the substrate. Explored were also the most probable mechanisms of the effects of changed gravity on the cell as a biomechanic structure. Specialized and non-specialized graviceptors of various types of cells were crypt-analyzed and classified. In future, investigations should be angled for elucidation of the role of intracellular components in perception and implementation of the gravitational stimulus, and description of quantitative characteristics of energy exchange and metabolism in cells as a function of gravity force and direction.

Biomechanical Phenomena↗
PubMed1984

Effect of 13-norleucin motilin on water and ion transport in the human jejunum.

Passage of the interdigestive migrating myoelectric complex through the proximal small bowel is associated with elevated plasma motilin levels and an increase in transmucosal potential difference suggesting altered ion transport. The aim of the present study was to investigate whether motilin may have an effect on intestinal water and ion transport. Steady state jejunal perfusion studies were carried out in healthy volunteers while either saline (control) or synthetic motilin (256 pmol/kg X h) was infused via peripheral vein. Plasma motilin levels rose from a mean of 31 to a plateau of 832 pmol/L. Motilin infusion significantly reduced absorption of water, sodium, potassium, and chloride when a plasmalike electrolyte solution was perfused. During perfusion with a bicarbonate-free salt solution, motilin significantly enhanced secretion of water, potassium, and chloride. Chloride secretion was active inasmuch as it occurred against both an electrical and chemical gradient. Motilin infusion had no effect on transit time during perfusion of the 30-cm jejunal test segments. We conclude that motilin can act as an intestinal secretagogue in the human jejunum.

Adolescent↗
PubMed1981

Hb Toyoake: beta 142 (H20) Ala replaced by Pro. A new unstable hemoglobin with high oxygen affinity.

A new unstable hemoglobin with high oxygen affinity, Hb Toyoake: beta 142 (H20) Ala replaced by Pro, was found in Japanese male with a normal blood hemoglobin level, shortened red cell survival, and increased plasma erythropoietin. Hemoglobin studies showed heat and isopropanol instability, and an increased tendency to heme loss and to subunit dissociation. Electrophoresis of whole hemolysate showed inconstant abnormal bands with reduced mobilities due to progressive heme loss during the in vitro procedure. Isolated Hb Toyoake with normal heme content migrated slightly faster than HbA. Oxygen affinity of red cells was elevated with P50 of 17.0 mm Hg at pH 7.4 and 37 degrees C (normal 25.0 mm Hg). Studies on hemolysate implied that Hb Toyoake had an almost normal Bohr effect, a diminished cooperativity, and a reduced response to inositol hexaphosphate. These multiple abnormalities are associated with a substitution of Pro for beta 142 Ala, resulting in disruption of the H-helix and the adjacent C-terminal portion of beta chain, which contain residues crucial for normal oxygen binding.

Adult↗
PubMed1998

Role of the ileocecal junction in the motor response to intestinal resection

Extensive resections of the distal small intestine are associated with motor disruption in the proximal remnant. Luminal contents such as bacteria and short-chain fatty acids may play a role. We evaluated the effect of bypass of the ileocecal junction (ICJ) on the motor response to a 50% distal resection. Thirty-five dogs were divided into three groups: transection control (TC, n = 11); 50% distal resection with intact ICJ (DR, n = 12), and 50% distal resection with jejunocolostomy to bypass the ICJ (DRBP, n = 12). Motor activity, intestinal transit, nutrition, absorption, and motor active hormones were studied over a 3-month period. Caloric intake was reduced and nutritional status similarly impaired in both resected groups. Steatorrhea, however, was significantly greater after DRBP. Intestinal structural adaptation was similar in both resected groups at 12 weeks. Animals in the bypass group demonstrated elevated intraluminal short-chain fatty acid and anaerobic bacterial counts. Migrating motor complex frequency was similar in the three groups; distal starts, however, were more frequent in both resected groups. Clustered contractile activity was prominent in the remnant after both DR and DRBP (50% and 32% recording time occupied by clusters, respectively [not significant]. Basal levels of peptide YY were increased following resection and this increase was unaffected by ICJ bypass. Postprandial neurotensin concentrations were transiently increased after distal bowel resection. In contrast, the postprandial neurotensin response was abolished following resection with bypass of the ICJ. Basal motilin levels were reduced following resection alone but not after resection with ICJ bypass. The motor response to resection does not appear to be related to alterations in circulating levels of hormones localized to the distal ileum; neither does it seem to be influenced by luminal bacteria and short-chain fatty acids or retention of a sphincteric mechanism at the ICJ. These findings also raise questions about the role of short-chain fatty acids and bacteria in the generation of the various distinctive motor patterns of the distal ileum. Resection of the distal ileum through loss of the receptor site for either retarding reflexes or bile salt absorption may be of greater importance in determining the motor response to resection.

Journal Article↗
PubMed2000

Induction of the urokinase plasminogen activator system by oncostatin M promotes endothelial migration.

Oncostatin M (OSM) is an inflammatory cytokine produced by activated macrophages and T-lymphocytes. We have previously demonstrated that OSM-induced endothelial cell migration, unlike endothelial cell proliferation and spindle formation, is independent of basic fibroblast growth factor expression (Wijelath et al. [1997] J. Cell. Sci. 110:871-879). To better understand the mechanism of OSM-induced endothelial cell migration, this study examined the potential role of the plasminogen activator system in promoting OSM mediated endothelial cell migration. OSM stimulated increased mRNA levels of urokinase-plasminogen activator (uPA) and urokinase-plasminogen activator receptor (uPAR) in a time and dose-dependent manner. Transcriptional run-off and mRNA stability analysis demonstrated that the increase in uPA and uPAR mRNA levels was due to both increased gene transcription and mRNA stability. The increase in mRNA correlated with increased protein levels of both uPA and uPAR. This increase was reflected in elevated levels of membrane-bound plasmin activity. OSM-induced endothelial cell migration was only partially dependent on plasmin activity since incubating endothelial cells without plasminogen or, in the presence of aprotinin, resulted in suppression of endothelial cell migration, indicating that OSM promoted endothelial cell migration through both a plasmin-dependent and -independent mechanism. Our results imply a role for OSM in promoting endothelial cell migration via a plasmin-dependent pathway and a uPAR-mediated pathway. Together, these and other recent studies support a role for OSM in modulating the different phases of angiogenesis.

Cells, Cultured↗
PubMed2004

Transport stress increases somatic cell counts in milk, and enhances the migration capacity of peripheral blood neutrophils of dairy cows.

The present study was designed to determine the effects of physiological stress on milk-somatic cell counts (SCC) and function of bovine peripheral blood leukocytes (PBL). Nine healthy lactating cows were used in the examination. Five cows were transported 100 km for 4 hr (transported group; TG), and 4 cows were penned (non-transported group; NTG). Blood and milk samples were collected at 0, 2, and 4 hr after loading, and at 2 hr, and 1, 2, 3, and 6 days after unloading. The following activities were measured: adhesion receptor (CD 18 and L-selectin) expression of neutrophils and monocytes, migration capacity and percentage of apoptotic cells of neutrophils, serum soluble L-selectin (sL-selectin), plasma cortisol, and SCC. A significant increase in plasma cortisol and milk SCC was observed in TG. Leukocytosis, derived from neutrophils was recorded in TG, and was indicated by apoptotic measurement as an increase of young cells from the marginal pool. Increased migration and decreased surface expression of both L-selectin and CD 18 in neutrophils were observed after transportation. Elevated serum sL-selectin was also noted as a result of transportation. The present study indicated that transport stress modulates peripheral blood neutrophil function, particularly enhancing migration capacity, and causes diapedesis across the mammary epithelium. Increased milk SCC in transported cattle might be due to these phenomena, and severe physiological stress may bring about an increase in SCC in milk.

Agriculture↗
PubMed2024

LINC00887 promotes GCN5-dependent H3K27cr level and CRC metastasis via recruitment of YEATS2 and enhancing ETS1 expression.

Recent observations have revealed upregulation of H3K27cr in colorectal cancer (CRC) tissues; however, the underlying cause remains elusive. This study aimed to investigate the mechanism of H3K27cr upregulation and its roles in CRC metastasis. Clinically, our findings showed that H3K27cr served as a highly accurate diagnostic marker to distinguish CRC tissues from healthy controls. Elevated levels of LINC00887 and H3K27cr were associated with a poorer prognosis in CRC patients. Functionally, LINC00887 and H3K27cr facilitated the migration and invasion of CRC cells. Mechanistically, LINC00887 interacted with SIRT3 protein. Overexpressed of LINC00887 obstructed the enrichment of SIRT3 within GCN5 promoter, thereby elevating H3K27ac but not H3K27cr level within this region, subsequently activating GCN5 expression. This activation increased the global level of H3K27cr, promoting the enrichment of GCN5, H3K27cr, and YEATS2 within ETS1 promoter, activating ETS1 transcription and ultimately promoting the metastasis of CRC. The in vivo study demonstrated that inhibition of LINC00887 suppressed CRC metastasis, but this inhibitory effect was nullified when mice were treated with NaCr. In conclusion, our results confirmed the diagnostic biomarker potential of H3K27cr in individuals with CRC, and proposed a functional model to elucidate the involvement of LINC00887 in promoting CRC metastasis by elevating H3K27cr level.

Humans↗
PubMed2004

Elevated levels of soluble adhesion molecules in sera of patients with acute bronchiolitis.

The mechanisms of migration of neutrophils into the airway lumen are crucial in the development of airway injury of acute bronchiolitis and are mediated by adhesion molecules. In this study, we have attempted to evaluate the role of serum concentrations of the soluble form of intercellular adhesion molecule-1 (sICAM-1) in the disease activity in acute bronchiolitis and in respiratory syncytial virus (RSV) infection. Circulating levels of sICAM-1 in sera from 10 normal control subjects, and from 47 hospitalized acute bronchiolitis patients at admission, and from 25 patients on the day of discharge were determined by use of commercially available enzyme-linked immunosorbent assay kits. The mean serum level of sICAM-1 in bronchiolitis patients was significantly higher than in the 10 healthy control infants (345.8 +/- 99.7 microg/mL vs 237.1 +/- 81.7 microg/mL; p<0.05). However, the mean sICAM-1 concentration was similar between RSV-positive and RSV-negative patients (337.5 +/- 99.6 microg/mL vs 350.9 +/- 101.1 microg/mL; p=0.65). Although the mean clinical severity score of RSV-positive patients was significantly higher than that of RSV-negative patients (5.94 +/- 1.83 vs 3.48 +/- 1.70; p<0.05). The improvement of clinical severity score was not well correlated with the change of sICAM-1 level (r=0.22). This study provides evidence that serum levels of sICAM-1 are increased in acute bronchiolitis and further confirms the role of adhesion molecules involved in the pathogenesis of the disease. However, the serum concentrations of the soluble adhesion molecules could not reliably reflect the clinical severity of the disease.

Acute Disease↗
PubMed2004

A3 adenosine receptor signaling contributes to airway inflammation and mucus production in adenosine deaminase-deficient mice.

Adenosine signaling has been implicated in chronic lung diseases such as asthma and chronic obstructive pulmonary disease; however, the specific roles of the various adenosine receptors in processes central to these disorders are not well understood. In this study, we have investigated the role(s) of the A(3) adenosine receptor in adenosine-dependent pulmonary inflammation observed in adenosine deaminase (ADA)-deficient mice. The A(3) receptor (A(3)R) was found to be expressed in eosinophils and mucus-producing cells in the airways of ADA-deficient mice. Treatment of ADA-deficient mice with MRS 1523, a selective A(3)R antagonist, prevented airway eosinophilia and mucus production. Similar findings were seen in the lungs of ADA/A(3) double knockout mice. Although eosinophils were decreased in the airways of ADA-deficient mice following antagonism or removal of the A(3)R, elevations in circulating and lung interstitial eosinophils persisted, suggesting signaling through the A(3)R is needed for the migration of eosinophils into the airways. These findings identify an important role for the A(3)R in regulating lung eosinophilia and mucus production in an environment of elevated adenosine.

Adenosine Deaminase↗
PubMed1986

Gene and teratogen induced defects of early central nervous system development.

The events involved in the histogenesis of the primitive nervous system involve precise control over cell shape changes, cellular migrations, cell-cell and cell-extracellular matrix interactions. The coordinated procession of these events results in the elevation of the neural folds, and their apposition and fusion in the dorsal midline, forming the primary neural tube. This is followed by a second series of cellular migrations and rearrangements (collectively called secondary neurulation) which result in lengthening of the caudal neural tube. After a brief consideration of the mechanisms involved in neurulation, the effects of gene or teratogen induced perturbations of these events are presented and reviewed. New data are presented on neurulation in the delayed Splotch mutant embryo and on the effects of altering mesenchymal or neuroepithelial basal lamina constituents on primary and secondary neurulation.

Animals↗
PubMed1987

Immune reactions in patients with type I and with type II diabetes mellitus.

Since several data refer to the role of immune processes in the pathogenesis of diabetes mellitus, this study was performed to compare aspecific and specific immune reactions in type I- and in type II diabetic patients over a six month period. The percentage and the absolute number of SRBC-rosette forming active E(A), of theophylline-resistant E(Thr) and of ORCB-rosette forming T(M)-cell subsets proved to be elevated in newly diagnosed type I but reduced in type II diabetic patients. Also an elevated percentage of HLA-DR positive, activated T cells was found in the majority of recent-onset type I diabetics. In the presence of human pancreas extract, a significant inhibition of leucocyte migration, a pronounced and specific cytotoxic capacity of all lymphocyte subsets (especially of the T(G)-cells), and elevated antibody titers (passive haemagglutination, indirect immunofluorescence) were observed in almost all type I diabetics, but only in a few cases of type II patients. After six months, the frequency both of the aspecific and of the specific immune parameters was decreased in type I diabetics, but no changes were observed in the type II diabetics with a previously positive test. The latter patients required insulin therapy at the time of the second investigation. The leucocyte migration inhibition test and the lymphocyte-mediated cytotoxicity are suitable for studying in-vitro-sensitization against pancreatic tissue and they might predict later insulin-dependency in type II diabetic patients.

Adolescent↗
PubMed2003

The canine mast cell activation via CRP.

We report here canine mastocytoma-derived cell (CMMC) activation via two pentraxin, limulus- and human-CRP. Mast cell chemotaxis was measured by Boyden's blindwell chamber. To confirm that the cell migration was chemotactic, "checkerboard" analysis was performed. We used Fura-2 to investigate CRP-mediated cytosolic calcium elevation. To examine whether CRP-induced stimulation is mediated through G-proteins, CMMC were incubated with pertussis toxin (PTx) before use in chemotaxis assay and Ca(2+) mobilization. CMMC migration in response to CRP was both chemokinetic and chemotactic. Limulus-CRP induced a transient Ca(2+)-mobilization dose-dependently. Preincubation of the cells with PTx inhibited CRP chemotaxis and Ca(2+)-mobilization, suggesting that G-proteins of the Gi-class are involved in the chemotaxis. We suggest that CRP may participate in the migration of mast cells to inflamed tissues during an acute-phase response. CRP-mediated recruitment of mast cells might play an important role in hypersensitivity and inflammatory processes.

Animals↗
PubMed1984

Mononuclear and polymorphonuclear leucocyte dysfunction in male homosexuals with the acquired immunodeficiency syndrome (AIDS).

In addition to the well-documented abnormalities of cell-mediated immunity we have observed that both polymorphonuclear leucocytes (PMNLs) and mononuclear leucocytes (MNLs) from 3 patients with the acquired immunodeficiency syndrome (AIDS) showed markedly defective migratory responsiveness to leuko-attractants in vitro. Reduced PMNL and MNL chemotaxis is attributable, at least in part, to a serum inhibitor of leucocyte migration, since co-incubation of PMNLs from healthy control subjects with 10% AIDS serum inhibited the migration to leuko-attractants of these cells. This serum-inhibitory effect on leucocyte migration was not due to the presence in AIDS serum of increased levels of prostaglandin E2, cytomegalo-virus or anti-leukocyte antibodies. However, elevated serum immunoglobulin A (IgA) levels were observed in all 3 patients. IgA is a potent inhibitor of PMNL and MNL migration. It is possible that serum inhibitors of leucocyte migration perpetuate the profound immunosuppression characteristic of AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed2004

Cdk5 regulates activation and localization of Src during corneal epithelial wound closure.

Recent studies have shown that Cdk5, a member of the cyclin-dependent-kinase family, regulates adhesion and migration in a mouse corneal epithelial cell line. Here, we extend these findings to corneal wound healing in vivo and examine the mechanism linking Cdk5 to cytoskeletal reorganization and migration. Cdk5 was overexpressed in the corneal epithelium of transgenic mice under control of the ALDH3 promoter. Elevated Cdk5 expression retarded corneal debridement wound closure in these animals and suppressed remodeling of the actin cytoskeleton. Conversely, the Cdk5 inhibitor, olomoucine, accelerated debridement wound healing in organ cultured eyes of normal mice, caused migrating cells to separate from the epithelial cell sheet, and increased the level of activated Src(pY416) along the wound edge. To explore the relationship between Cdk5 and Src in greater detail, we examined scratch-wounded cultures of corneal epithelial cells. Src was activated in cells along the wound edge and blocking this activation with the Src kinase inhibitor, PP1, inhibited wound closure by 85%. Inhibiting Cdk5 activity with olomoucine or a dominant negative construct, Cdk5T33, increased the concentration of Src(pY416), shifted its subcellular localization to the cell periphery and enhanced wound closure. Cdk5(pY15), an activated form of Cdk5, also appeared along the wound edge. Inhibiting Src activity with PP1 blocked the appearance of Cdk5(pY15), suggesting that Cdk5 phosphorylation is Src dependent. Cdk5 and Src co-immunoprecipitated from scratch-wounded cultures, demonstrating that both kinases are part of an intracellular protein complex. These findings indicate that Cdk5 exerts its effects on cell migration during corneal epithelial wound healing by regulating the activation and localization of Src.

Actin Cytoskeleton↗