title: Expression of TGFbeta2 but not TGFbeta1 correlates with the deposition of scar tissue in the lesioned spinal cord.
abstract: Transforming growth factor-betas (TGFbetas) are implicated in fibrotic pathologies. TGFbeta1 and -beta2 expression is increased around the glial/fibrotic scar in the injured brain. Moreover, local injection of TGFbeta antagonists into cerebral wounds reduces glial scarring. Here, we monitored expression of TGFbeta1 and -beta2 mRNA and protein in the spinal cord after transection of the dorsal funiculi. Levels of TGFbeta1 mRNA were most elevated over the acute inflammatory phase, while TGFbeta2 mRNA levels were raised locally about the wound, particularly in astrocytes and neovascular endothelial cells, over the subacute period of scarring. TGFbeta protein production also increased after injury. Both TGFbeta1 and TGFbeta2 were found in hematogenous inflammatory cells, while TGFbeta1 was also neuron-associated, and high levels of TGFbeta2 were localized to multiple cell types in the wound, including reactive astrocytes, during the period of glial/collagen scar formation. The cellular localization and temporal pattern of expression of TGFbeta after spinal cord injury suggest that TGFbeta1 modulates the inflammatory and neuronal responses, while TGFbeta2 regulates glial/collagen scarring.
authors.affiliation: Department of Medicine, Wolfson Research Laboratories, Queen Elizabeth Medical Centre, University of Birmingham, Edgbaston, United Kingdom.
authors.forename: C
authors.initials: C
authors.lastname: Lagord
authors.forename: M
authors.initials: M
authors.lastname: Berry
authors.forename: A
authors.initials: A
authors.lastname: Logan
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000166:cytology / Q000378:metabolism*; D001808:Blood Vessels / Q000166:cytology / Q000378:metabolism; D002921:Cicatrix / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D003094:Collagen / Q000378:metabolism; D004195:Disease Models, Animal; D005109:Extracellular Matrix / Q000378:metabolism; D005260:Female; D005347:Fibroblasts / Q000378:metabolism; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D007249:Inflammation / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D007797:Laminin / Q000378:metabolism; D008264:Macrophages / Q000166:cytology / Q000378:metabolism; D008578:Meninges / Q000166:cytology / Q000378:metabolism; D009389:Neovascularization, Pathologic / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D009474:Neurons / Q000166:cytology / Q000378:metabolism; D009836:Oligodendroglia / Q000166:cytology / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013119:Spinal Cord Injuries / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000378:metabolism*; D053773:Transforming Growth Factor beta1; D053781:Transforming Growth Factor beta2; D015854:Up-Regulation / Q000502:physiology; D014945:Wound Healing / Q000502:physiology
chemical_list: D005904:Glial Fibrillary Acidic Protein; D007797:Laminin; D012333:RNA, Messenger; C508962:Tgfb1 protein, rat; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1; D053781:Transforming Growth Factor beta2; D003094:Collagen