Sung-Woo Ha

Beta ig-h3 promotes renal proximal tubular epithelial cell adhesion, migration and proliferation through the interaction with α3β1 integrin

Betaig-h3 (βig-h3) is a secretory protein composed of fasciclin I-like repeats containing sequences that allows binding of integrins and glycosaminoglycans in vivo. Expression of βig-h3 is responsive to TGF-β and the protein is found to be associated with extracellular matrix (ECM) molecules, implicating βig-h3 as an ECM adhesive protein of developmental processes. We previously observed predominant expression of βig-h3 expression in the basement membrane of proximal tubules of kidney. In this study, the physiological relevance of such localized expression of βig-h3 was examined in the renal proximal tubular epithelial cells (RPTEC). RPTEC constitutively expressed βig-h3 and the expression was dramatically induced by exogenous TGF-β1 treatment. βig-h3 and its second and fourth FAS1 domain were able to mediate RPTEC adhesion, spreading and migration. Two known α3β1 integrin-interaction motifs including aspartatic acid and isoleucine residues, NKDIL and EPDIM in βig-h3 were responsible to mediate RPTEC adhesion, spreading, and migration. By using specific antibodies against integrins, we confirmed that α3β1 integrin mediates the adhesion and migration of RPTECs on βig-h3. In addition, it also enhanced proliferation of RPTECs through NKDIL and EPDIM. These results indicate that βig-h3 mediates adhesion, spreading, migration and proliferation of RPTECs through the interaction with α3β1 integrin and is intimately involved in the maintenance and the regeneration of renal proximal tubular epithelium.

Factors that Affect Medication Adherence in Elderly Patients with Diabetes Mellitus

Background This study was conducted to evaluate the factors affecting medication adherence in geriatric diabetic patients treated at private clinics and tertiary hospitals. We compared the factors affecting medication adherence between these two patient groups. Methods We included 108 diabetic patients older than 65 years treated at one tertiary hospital and 157 patients older than 65 years treated at two private clinics. We conducted an interview survey based on the Health Belief Model, and used a questionnaire that included the self-efficacy variable. For the medication adherence, Moriskys self-report was used. Results The medication adherence based on Moriskys self-report was significantly higher in tertiary hospital patients (61.1%) compared to private clinic patients (43.2%) (P < 0.01). The results showed that drug storage and self-efficacy were factors affecting adherence to medication in tertiary hospital patients (P < 0.05). The adherence was high in cases of proper drug storage (odds ratio [OR], 5.401) and in cases with high self-efficacy (OR, 13.114). In private clinic patients, financial level (P < 0.05), recognition of the seriousness of diabetes complications (P < 0.05) and self-efficacy (P < 0.01) were associated with medication adherence. The medication adherence was significantly lower in patients whose financial state were moderate than those with lower (OR, 0.410), and medication adherence was significantly higher in patients who had higher perceived severity (OR, 2.936) and in patients with higher self-efficacy (OR, 4.040). Conclusion Different strategies should be used to increase medication adherence in geriatric diabetic patients, depending on institutions whether they are treated.

TGF‐β‐induced protein βig‐h3 is upregulated by high glucose in vascular smooth muscle cells

TGF‐β‐induced gene‐h3 (βig‐h3) is an adhesive molecule that interacts with integrins. Because TGF‐β plays an important role in diabetic complications and βig‐h3 serves as a cell substrate, we hypothesized that diabetic conditions might increase βig‐h3 synthesis in vascular smooth muscle cells (VSMCs), which may subsequently contribute to the pathogenesis of diabetic angiopathy. The concentrations of βig‐h3 and TGF‐β were measured in conditioned media using an enzyme‐linked immunosorbent assay. An immunohistochemical study showed that βig‐h3 was expressed in the VSMCs and the matrix of rat aortas. TGF‐β stimulated βig‐h3 production, and high glucose induced βig‐h3 as well as TGF‐β production in the VSMCs. The high glucose‐induced βig‐h3 expression was almost entirely blocked by an anti‐TGF‐β antibody. βig‐h3 protein mediated the adhesion, spreading, migration, and proliferation of rat VSMCs. These results suggest that the high glucose‐induced βig‐h3 in VSMCs regulates VSMC functions and may play an important role in diabetic angiopathy.