Transforming growth factor-β1 exhibits delayed gene expression following focal cerebral ischemia

• Published in: Brain research bulletin Vol. 36; no. 6; pp. 607 - 609
• Main Authors: Wang, Xinkang, Yue, Tian-Li, White, Raymond F., Barone, Frank C., Feuerstein, Giora Z.
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 1995; Elsevier Science
• Subjects: Biological and medical sciences; Cytokines; Focal brain ischemia; Medical sciences; Neurology; Rats; TGFβ1; Vascular diseases and vascular malformations of the nervous system; Rats; TGFβ1; Cytokines; Focal brain ischemia; Nervous system diseases; Rat; Transforming growth factor β; Rodentia; Central nervous system; Cytokine; Gene expression; Vertebrata; Experimental disease; Mammalia; Ischemia; Animal; Transforming growth factor β1; Cerebrovascular disease; Brain (vertebrata)
• ISSN: 0361-9230; 1873-2747
• DOI: 10.1016/0361-9230(94)00243-T

Transforming growth factor-β1 (TGF-β1) is a pleiotropic peptide growth factor. The expression of TGF-β1 mRNA in the focal ischemic cortex of rats was studied by means of Northern hybridization. A moderately low level of constitutively expressed TGF-β1 mRNA was detected following ohm surgery or in the contralateral (nonlschemic) cortex. A significant increase of TGF-β1 mRNA level in the ischemic cortex was observed at 2 days (3.2-fold increase compared to sham-operated animals, p < 0.01, n = 4) following permanent occlusion of the middle cerebral artery (PMCAO). The elevated TGF-μ1 mRNA expression was plateaued for up to 16 days (3–6-fold increase, p < 0.01) following PMCAO- This temporal profile for TGF-β1 mRNA expression in focal stroke was significantly delayed compared to that of TNF-α, IL-1β and IL-6 MRNA expressions as demonstrated previously which peaked at 12 h and decreased to almost basal levels by S days following PMCAO. Interestingly, the TGF-β1 mRNA expression profile was remarkably parallel with that of monocyte/macrophage accumulation in the ischemic cortex, as well as with the increased formation of extracellular matrix in the focal ischemic brain. These data suggest that TGF-β1 may play a role in anti-inflammatory process and in tissue remodeling following ischernic brain injury.