EXPRESS: Oligodendrocytes in HIV-associated pain pathogenesis

• Published in: Molecular pain 2016, Vol.12
• Main Authors: Shi, Yuqiang, Shu, Jianghong, Liang, Zongsuo, Yuan, Subo, Tang, Shao-Jun
• Format: Article
• Language: English
• Subjects: Animals; Biomarkers - metabolism; Gene Knockdown Techniques; HIV Envelope Protein gp120 - metabolism; HIV Infections - complications; HIV Infections - metabolism; HIV Infections - pathology; Humans; Hyperalgesia - metabolism; Hyperalgesia - pathology; Mice, Inbred C57BL; Mice, Knockout; Myelin Basic Protein - metabolism; Myelin Sheath - metabolism; Oligodendroglia - metabolism; Oligodendroglia - pathology; Pain - etiology; Pain - metabolism; Pain - pathology; Spinal Cord Dorsal Horn - metabolism; Spinal Cord Dorsal Horn - pathology; Up-Regulation
• ISSN: 1744-8069
• DOI: 10.1177/1744806916656845

Although the contributions of microglia and astrocytes to chronic pain pathogenesis have been a focal point of investigation in recent years, the potential role of oligodendrocytes, another major type of glial cells in the CNS that generates myelin, remains largely unknown. We report here that cell markers of the oligodendrocyte lineage, including NG2, PDGFRa, and Olig2, are significantly increased in the spinal dorsal horn of HIV patients who developed chronic pain. The levels of myelin proteins myelin basic protein and proteolipid protein are also aberrant in the spinal dorsal horn of "pain-positive" HIV patients. Similarly, the oligodendrocyte and myelin markers are up-regulated in the spinal dorsal horn of a mouse model of HIV-1 gp120-induced pain. Surprisingly, the expression of gp120-induced mechanical allodynia appears intact up to 4 h after myelin basic protein is knocked down or knocked out. These findings suggest that oligodendrocytes are reactive during the pathogenesis of HIV-associated pain. However, interfering with myelination does not alter the induction of gp120-induced pain.