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Shh

[Sonic hedgehog] Shh is a member of the hedgehog gene family comprising Sonic hegehog, Indian hedgehog, and Desert hedgehog. The mammalian factors encoded by these genes are homologs of a Drosophila melanogaster gene that regulates pattern formation. The mammalian gene products are secreted factors that play an important role in morphogenesis, particularly during embryonic development, controlling many critical steps of cell differentiation and patterning. The receptor has been identified as patched.

Tavella et al (2004) have generated transgenic mice overexpressing human Sonic hedgehog in chondrocytes. Overexpression causes a lethal craniorachischisis and other skeletal defects in ribs, sternum, and long bones because of defects in chondrocyte differentiation. Overexpression also causes an increase in its receptor, patched and a reduction in the expression of Indian hedgehog, which is known also to influence chondrocyte development. Overexpression of Sonic hedgehog also causes upregulation of the expression of Sox9, a major transcription factor implicated in chondrocyte-specific gene expression.

Sacedon et al (2005) have reported that Shh is produced by follicular dendritic cells and protects germinal center B-cells from apoptosis.

Straface et al (2008) have reported that the Sonic hedgehog signaling pathway is not silent in post-natal life. The protein and its receptor are expressed de novo after injury and during regeneration of the adult skeletal muscle. This plays an important regulatory role on injury-induced angiogenesis, as inhibition of Shh function results in impaired upregulation of prototypical angiogenic agents, such as VEGF and SDF-1-alpha, decreased muscle blood flow, and reduced capillary density after injury. Shh reactivation plays a regulatory role also on myogenesis, as its inhibition impairs the activation of the myogenic regulatory factors Myf-5 and MyoD, decreases the upregulation of IGF-1, and reduces the number of myogenic satellite cells at injured site. Shh inhibition results in muscle fibrosis, increased inflammatory reaction, and compromised motor functional recovery after injury.

LAST MODIFIED: August 2008

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