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Thymosin Beta 4(TB-500) Injury Healing
- Thread starter John Juan
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John Juan
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Over-expression of thymosin beta 4 promotes abnormal tooth development and stimulation of hair growth.
AuthorsCha HJ, et al. Show all Journal
Int J Dev Biol. 2010;54(1):135-40. doi: 10.1387/ijdb.082735hc.
Affiliation
Abstract
Thymosin beta 4 has multi-functional roles in cell physiology. It accelerates wound healing, hair growth and angiogenesis, and increases laminin-5 expression in corneal epithelium. Furthermore, thymosin beta 4 stimulates tumor growth and metastasis by induction of cell migration and vascular endothelial growth factor-mediated angiogenesis. Using a construct on the skin-specific keratin-5 promoter, we have developed thymosin beta 4 over-expressing transgenic mice to further study its functional roles. Thymosin beta 4 in adult skin and in embryonic stages of the transgenic mouse was analyzed by both Western blot and immunohistochemistry. The over-expression of thymosin beta 4 was observed especially around hair follicles and in the teeth in the transgenic mice. We examined the phenotype of the thymosin beta 4 over-expressing mice. Hair growth was accelerated. In addition, the transgenic mice had abnormally-shaped white teeth and dull incisors. We found that the expression of laminin-5 was up-regulated in the skin of the transgenic mice. We conclude that thymosin beta 4 has an important physiological role in hair growth and in tooth development.
AuthorsCha HJ, et al. Show all Journal
Int J Dev Biol. 2010;54(1):135-40. doi: 10.1387/ijdb.082735hc.
Affiliation
Abstract
Thymosin beta 4 has multi-functional roles in cell physiology. It accelerates wound healing, hair growth and angiogenesis, and increases laminin-5 expression in corneal epithelium. Furthermore, thymosin beta 4 stimulates tumor growth and metastasis by induction of cell migration and vascular endothelial growth factor-mediated angiogenesis. Using a construct on the skin-specific keratin-5 promoter, we have developed thymosin beta 4 over-expressing transgenic mice to further study its functional roles. Thymosin beta 4 in adult skin and in embryonic stages of the transgenic mouse was analyzed by both Western blot and immunohistochemistry. The over-expression of thymosin beta 4 was observed especially around hair follicles and in the teeth in the transgenic mice. We examined the phenotype of the thymosin beta 4 over-expressing mice. Hair growth was accelerated. In addition, the transgenic mice had abnormally-shaped white teeth and dull incisors. We found that the expression of laminin-5 was up-regulated in the skin of the transgenic mice. We conclude that thymosin beta 4 has an important physiological role in hair growth and in tooth development.
John Juan
New member
Thymosin beta 4 sulfoxide is an anti-inflammatory agent generated by monocytes in the presence of glucocorticoids.
AuthorsYoung JD, et al. Show all Journal
Nat Med. 1999 Dec;5(12):1424-7.
Affiliation
Abstract
The possibility that glucocorticoids upregulate the expression of anti-inflammatory mediators is an exciting prospect for therapy in inflammatory diseases, because these molecules could give the therapeutic benefits of steroids without toxic side effects. Supernatants from monocytes and macrophages cultured in the presence of glucocorticoids increase the dispersion of neutrophils from a cell pellet in the capillary tube migration assay. This supernatant factor, unlike other neutrophil agonists, promotes dispersive locomotion of neutrophils at uniform concentration, lowers their adhesion to endothelial cells, inhibits their chemotactic response to fMLP and induces distinctive morphological changes. Here we show that thymosin beta4 sulfoxide is generated by monocytes in the presence of glucocorticoids and acts as a signal to inhibit an inflammatory response. In vitro, thymosin beta4 sulfoxide inhibited neutrophil chemotaxis, and in vivo, the oxidized peptide, but not the native form, was a potent inhibitor of carrageenin-induced edema in the mouse paw. Thymosin beta4 is unique, because oxidation attenuates its intracellular G-actin sequestering activity, but greatly enhances its extracellular signaling properties. This description of methionine oxidation conferring extracellular function on a cytosolic protein may have far-reaching implications for future strategies of anti-inflammatory therapy.
AuthorsYoung JD, et al. Show all Journal
Nat Med. 1999 Dec;5(12):1424-7.
Affiliation
Abstract
The possibility that glucocorticoids upregulate the expression of anti-inflammatory mediators is an exciting prospect for therapy in inflammatory diseases, because these molecules could give the therapeutic benefits of steroids without toxic side effects. Supernatants from monocytes and macrophages cultured in the presence of glucocorticoids increase the dispersion of neutrophils from a cell pellet in the capillary tube migration assay. This supernatant factor, unlike other neutrophil agonists, promotes dispersive locomotion of neutrophils at uniform concentration, lowers their adhesion to endothelial cells, inhibits their chemotactic response to fMLP and induces distinctive morphological changes. Here we show that thymosin beta4 sulfoxide is generated by monocytes in the presence of glucocorticoids and acts as a signal to inhibit an inflammatory response. In vitro, thymosin beta4 sulfoxide inhibited neutrophil chemotaxis, and in vivo, the oxidized peptide, but not the native form, was a potent inhibitor of carrageenin-induced edema in the mouse paw. Thymosin beta4 is unique, because oxidation attenuates its intracellular G-actin sequestering activity, but greatly enhances its extracellular signaling properties. This description of methionine oxidation conferring extracellular function on a cytosolic protein may have far-reaching implications for future strategies of anti-inflammatory therapy.
Elvia1023
New member
I modified my leg training I haven't really had anymore knee issues so never bought this. Pretty much everyone I have read about using this as had great results. I am lifting much lighter in general so hopefully that will prevent any bad injuries. Although if I ever injure myself badly I will be jumping on this.
John Juan
New member
Thymosin β4 enhances the healing of medial collateral ligament injury in rat.
AuthorsXu B, et al. Show all Journal
Regul Pept. 2013 Jun 10;184:1-5. doi: 10.1016/j.regpep.2013.03.026. Epub 2013 Mar 21.
Affiliation
Abstract
The role played by thymosin β4 (Tβ4) in the process of wound healing was reported in several organs. However, there have been no reports that investigated the role of Tβ4 in the repair process after ligament injury. The purpose of this study was to determine whether administration of Tβ4 would improve ligament repair following injury. The medial collateral ligament (MCL) was sharply transected on the day of surgery. Then, the treatment group received 100 μL of fibrin sealant containing 1 μg of Tβ4 placed in the ligament gap. Healing tissues were evaluated by hematoxylin and eosin stain, transmission electron microscopy, and biomechanical test at 4 weeks after surgery. Histologically, healing tissues in Tβ4-treated group exhibited uniform and evenly spaced fiber bundles. However, the collagen fibers were not evenly spaced in control rats. Moreover, diameters of collagen fibrils within granulation tissue from the Tβ4-treated rats were significantly increased. In Tβ4-treated MCLs, the mechanical properties of these healing tissues were significantly higher at 4 weeks after surgery. In terms of the mechanical properties of the healing femur-medial collateral ligament-tibia complexes, the Tβ4-treated group had significantly better biomechanical properties than the control group at 4 weeks after surgery. Local administration of Tβ4 promotes the healing process of MCL, both histologically and mechanically, in a rat model. These findings provide a basis for potential clinical use of Tβ4 in repairing ligaments.
AuthorsXu B, et al. Show all Journal
Regul Pept. 2013 Jun 10;184:1-5. doi: 10.1016/j.regpep.2013.03.026. Epub 2013 Mar 21.
Affiliation
Abstract
The role played by thymosin β4 (Tβ4) in the process of wound healing was reported in several organs. However, there have been no reports that investigated the role of Tβ4 in the repair process after ligament injury. The purpose of this study was to determine whether administration of Tβ4 would improve ligament repair following injury. The medial collateral ligament (MCL) was sharply transected on the day of surgery. Then, the treatment group received 100 μL of fibrin sealant containing 1 μg of Tβ4 placed in the ligament gap. Healing tissues were evaluated by hematoxylin and eosin stain, transmission electron microscopy, and biomechanical test at 4 weeks after surgery. Histologically, healing tissues in Tβ4-treated group exhibited uniform and evenly spaced fiber bundles. However, the collagen fibers were not evenly spaced in control rats. Moreover, diameters of collagen fibrils within granulation tissue from the Tβ4-treated rats were significantly increased. In Tβ4-treated MCLs, the mechanical properties of these healing tissues were significantly higher at 4 weeks after surgery. In terms of the mechanical properties of the healing femur-medial collateral ligament-tibia complexes, the Tβ4-treated group had significantly better biomechanical properties than the control group at 4 weeks after surgery. Local administration of Tβ4 promotes the healing process of MCL, both histologically and mechanically, in a rat model. These findings provide a basis for potential clinical use of Tβ4 in repairing ligaments.
John Juan
New member
Myocardial regeneration: expanding the repertoire of thymosin β4 in the ischemic heart.
AuthorsSmart N, et al. Show all Journal
Ann N Y Acad Sci. 2012 Oct;1269:92-101. doi: 10.1111/j.1749-6632.2012.06708.x.
Affiliation
Abstract
Efficient cardiac regeneration postinfarction (MI) requires the replacement of lost cardiomyocytes, formation of new coronary vessels and appropriate modulation of the inflammatory response. However, insight into how to stimulate repair of the human heart is currently limited. Using the embryonic paradigm of regeneration, we demonstrated that the actin-binding peptide thymosin β4 (Tβ4), required for epicardium-derived coronary vasculogenesis, can recapitulate its embryonic role and activate quiescent adult epicardial cells (EPDCs). Once stimulated, EPDCs facilitate neovascularization of the ischemic adult heart and, moreover, contribute bona fide cardiomyocytes. EPDC-derived cardiomyocytes structurally and functionally integrate with resident muscle to regenerate functional myocardium, limiting pathological remodeling, and effecting an improvement in cardiac function. Alongside pro-survival and anti-inflammatory properties, these regenerative roles, via EPDCs, markedly expand the range of therapeutic benefits of Tβ4 to sustain and repair the myocardium after ischemic damage.
AuthorsSmart N, et al. Show all Journal
Ann N Y Acad Sci. 2012 Oct;1269:92-101. doi: 10.1111/j.1749-6632.2012.06708.x.
Affiliation
Abstract
Efficient cardiac regeneration postinfarction (MI) requires the replacement of lost cardiomyocytes, formation of new coronary vessels and appropriate modulation of the inflammatory response. However, insight into how to stimulate repair of the human heart is currently limited. Using the embryonic paradigm of regeneration, we demonstrated that the actin-binding peptide thymosin β4 (Tβ4), required for epicardium-derived coronary vasculogenesis, can recapitulate its embryonic role and activate quiescent adult epicardial cells (EPDCs). Once stimulated, EPDCs facilitate neovascularization of the ischemic adult heart and, moreover, contribute bona fide cardiomyocytes. EPDC-derived cardiomyocytes structurally and functionally integrate with resident muscle to regenerate functional myocardium, limiting pathological remodeling, and effecting an improvement in cardiac function. Alongside pro-survival and anti-inflammatory properties, these regenerative roles, via EPDCs, markedly expand the range of therapeutic benefits of Tβ4 to sustain and repair the myocardium after ischemic damage.
