Hepatocyte cytoplasmic OPN and HMGB1 expression was significant while loss of nuclear HMGB1 occurred in patients with HCV-induced fibrosis compared with healthy explants.Well-established liver fibrosis along with marked induction of HMGB1 occurred in CCl-induced liver fibrosis.
To this end, we analysed the expression of OPN and HMGB1 in paraffin-embedded archived human liver biopsies from deidentified controls and from patients with clinically proven hepatitis C virus (HCV).High-mobility group box-1 (HMGB1) is a nuclear non-histone chromosomal protein that binds the DNA minor groove and is involved in DNA replication, repair and energy homeostasis.4 Initially, it was believed that HMGB1 acted primarily as an architectural protein.However, upon cellular injury and post-translational modifications (PTMs), HMGB1 undergoes translocation from the nucleus to the cytoplasm and is secreted via the lysosomal pathway in most cells.5 HMGB1 signals via the receptor for advanced glycation end-products (RAGE), toll-like receptors (TLRs)-2/4/9, Mac-1, syndecan-1, phosphacan protein-tyrosine phosphatase-ζ/β and CD24.6Recent work from our laboratory has demonstrated that HMGB1 has noxious effects in the hepatic environment in the setting of alcoholic liver disease.7 When released from injured or necrotic cells due to loss of membrane integrity8 or when secreted by hepatocytes in response to ethanol,7 HMGB1 can trigger harmful responses.The algorithm is described in the ISO 3309 standard. It is not in any way intended to be used as a substitute for professional medical advice, diagnosis, treatment or care. Cyclic redundancy and other checksums Numerical recipes in C 2nd ed., pp896-902, Cambridge University Press (1993)) This subsection of the ‘Sequence’ section reports difference(s) between the canonical sequence (displayed by default in the entry) and the different sequence submissions merged in the entry. This subsection of the ‘Sequence’ section describes the sequence of naturally occurring alternative protein isoform(s).