Premium
Ubiquitin C‐terminal hydrolase‐L1 (PGP9.5) expression in human neural cell lines following induction of neuronal differentiation and exposure to cytokines, neurotrophic factors or heat stress
Author(s) -
Satoh J.I.,
Kuroda Y.
Publication year - 2001
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1046/j.1365-2990.2001.00313.x
Subject(s) - biology , synaptophysin , neurotrophic factors , cell culture , sh sy5y , retinoic acid , microbiology and biotechnology , cellular differentiation , neuroblastoma , biochemistry , immunology , immunohistochemistry , receptor , gene , genetics
Dysfunction of the ubiquitin‐dependent proteolytic pathway contributes to progressive accumulation of ubiquitinated protein inclusions in neurodegenerative disorders, such as Parkinson's disease (PD). Ubiquitin C‐terminal hydrolase‐L1 (UCH‐L1), alternatively designated protein gene product 9.5 (PGP9.5), is a neural deubiquitinating enzyme which is identified as a principal constituent of Lewy bodies. To clarify the regulatory mechanism of UCH‐L1 expression in human neural cells, we studied the constitutive, cytokine/neurotrophic factor‐regulated, and heat stress‐induced expression of UCH‐L1 in cultured human neural cell lines by Western blot analysis. The constitutive expression of UCH‐L1 was identified in SK‐N‐SH neuroblastoma cells, IMR‐32 neuroblastoma cells, U‐373MG astrocytoma cells, and NTera2 teratocarcinoma‐derived differentiated neurones (NTera2‐N). The levels of UCH‐L1 expression were unaltered in these cell lines following treatment with TNF‐α, IL‐1β, BDNF, GDNF, dibutyryl cyclic AMP, or phorbol 12‐myristate 13‐acetate, and remained unchanged by exposure to heat stress. In contrast, its levels were elevated substantially in NTera2 teratocarcinoma cells following retinoic acid‐induced neuronal differentiation, accompanied with an increased expression of α‐synuclein and synaptophysin. These results indicate that UCH‐L1 is expressed constitutively in human neual cell lines, where it is upregulated following induction of neuronal differentiation, but unaffected by exposure to heat stress, cytokines, or growth/differentiation factors which are supposed to be invloved in the nigral neuronal death and survival in PD.