Reduced Expression of Osteonectin and Increased Natural Killer Cells May Contribute to the Pathophysiology of Aplastic Anemia. Issue 2 (February 2015)

• Record Type: Journal Article
• Authors: Park, Meerim; Park, Chan-Jeoung; Jang, Seongsoo; Kim, Dae-Young; Lee, Jung-Hee; Lee, Je-Hwan; Lee, Kyoo-Hyung; Hwang, Kyoujung; Lee, Young Ho
• Is Part Of: Applied immunohistochemistry & molecular morphology. Volume 23:Issue 2(2015)
• Publication Date: 2015-02
• Subjects: aplastic anemia -- bone marrow microenvironment -- nestin -- natural killer cell; Diagnostic immunohistochemistry -- Periodicals; Immunohistochemistry -- Periodicals; Cells -- Morphology -- Periodicals; Molecular diagnosis -- Periodicals; 616.079
• DOI: 10.1097/PAI.0000000000000023
• Languages: English
• ISSNs: 1541-2016

Abstract

Abstract : Normal hematopoiesis involves complex interactions between hematopoietic cells and the bone marrow (BM) microenvironment. The exact causes and mechanisms involved in aplastic anemia (AA) are not known. For better understanding of the pathophysiology of AA, we investigated changes in the hematopoietic stem cell (HSC) compartment and the BM microenvironment in patients with AA by immunohistochemical analysis. A total of 10 AA patients and 10 controls were enrolled. Using BM biopsy specimen, we performed immunohistochemistry for osteopontin, osteonectin, osteocalcin, nestin, stromal-derived factor-1 (SDF-1), lymphocytes, macrophage, and HSCs. Numbers of HSCs and T/B lymphocytes were significantly lower in the AA specimens than the controls, and the AA specimens contained more natural killer cells (CD56 + cells) ( P <0.01). The 2 groups had similar levels of expression of osteopontin, osteocalcin, nestin, and SDF-1. However, the number of osteonectin + cells in the AA specimens was significantly lower than in the control specimens ( P <0.01). Our findings support the hypothesis that defects in the stromal cells contribute to the pathogenesis of AA by damaging HSC niche. Immune-mediated natural killer cells may also play a role in the pathogenesis of AA.