4.3 Article

Changes in CLIP3 expression after sciatic nerve injury in adult rats

Journal

JOURNAL OF MOLECULAR HISTOLOGY
Volume 43, Issue 6, Pages 669-679

Publisher

SPRINGER
DOI: 10.1007/s10735-012-9450-y

Keywords

Sciatic nerve injury; Schwann cells; Proliferation; Myelination; Degeneration; CLIP3

Categories

Funding

  1. National Natural Science Foundation of China [81171140, 30300099, 30770488, 30870320]
  2. Natural Science Foundation of Jiangsu province [BK2009161, BK2009156, BK200 9157]
  3. Natural science Foundation of Jiangsu Colleges and Universities [09KJD310005]
  4. Society and Technology Grew Project of Nantong City [S2008020]

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CLIP3 (cytoplasmic linker protein 3) is a 547 amino acid residue cytoplasmic protein that localises to Golgi stacks and tubulovesicular elements juxtaposed to Golgi cisternae. Composed of three Ank (ankyrin) repeats and two CAP-Gly (cytoskeleton-associated protein-glycine) domains, CLIP3 may function as a cytoplasmic linker protein that is involved in TGN-endosome dynamics. To define the expression and role of CLIP3 during peripheral nervous system degeneration and regeneration, we created an acute sciatic nerve injury (SNI) model in adult rats. Western blot analyses revealed prominent up-regulation of CLIP3 and PCNA (proliferating cell nuclear antigen) protein levels at 3 days after SNI. Immunohistochemistry displayed that the expression of CLIP3 was noticeably increased in the injured nerve. Immunofluorescence further revealed that the CLIP3 and PCNA proteins colocalised respectively with S100 in the cytoplasm of Schwann cells. The expression profile of the SC/neuron co-cultures demonstrated that CLIP3 and PCNA protein levels were markedly expressed during the early stage of myelination. These results suggest that CLIP3 is likely associated with the myelination of proliferating Schwann cells, and nerve tissue regeneration after peripheral nerve injury. CLIP3 and PCNA expression during early myelination may be related to the direct uptake and transport of lipids and cholesterol, which were derived from the degenerating myelin, by Schwann cells to prepare for the formation of myelin sheath-like structures around regenerated axons after SNI.

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