Glial scar shown to stimulate growth-inhibitory proteoglycans by astrocytes. Experimental reduction of TGFβ-1 and TGFβ-2 has been shown to partially reduce glial scarring. Interleukins are another potential family of scar-inducing cellular messengers. Particularly, interleukin-1, a protein produced by mononuclear phagocytes, helps to initiate the inflammatory response in astrocytes, leading to reactive astrogliosis and the formation of the glial scar. The cytokine family of glial scar inducers include interferon-γ (IFNγ) and fibroblast growth factor 2 (FGF2). IFNγ has been shown to induce astrocyte proliferation and increase the extent of glial scarring in injured brain models. Further, FGF2 production increases after injury to the
Carotid body sustentacular supportive cells. The carotid body contains the most vascularized tissue in the human body . The thyroid gland is very vascular, but not quite as much as the carotid body. The carotid body functions as a sensor: it responds to a stimulus, primarily O partial pressure, which is detected by the type I (glomus) cells, and triggers an action potential through the afferent fibers of the glossopharyngeal nerve, which relays the information to the central nervous system. The carotid body chemoreceptors are primarily sensitive to decreases in the partial pressure of oxygen (P). This is in contrast to the