Charles rundle | va loma linda health care | veterans affairs

My major research interest is analysis of molecular regulation of bone repair and development of novel therapeutic strategies to promote bone fracture healing. A significant proportion of

bone injuries fail to heal adequately, resulting in substantial health-related and economic consequences. Veterans experience impaired bone repair at frequencies even greater than the

general US population. My lab studies the repair of fractures of the long bones, with the objective of characterizing the molecular pathways that regulate bone formation and remodeling

during fracture repair. Ultimately, these studies will facilitate the development of novel therapeutic approaches for improving bone repair in conditions of impaired healing among veterans

and non-veteran patients. Previous studies have characterized fracture healing in knockout strains of mice, in which a gene of interest is genetically deleted. Selected mouse strains

examined to date have included “plasminogen activator inhibitor” and ephrin-B1 gene deletions. The effect of the gene deficiency is characterized by radiologic, histologic and the molecular

analysis of gene and protein expression during healing. These efforts have helped to characterize plasminogen axis regulation of extracellular tissues in fracture healing, and ephrin

communication in the development of the fracture callus. Mouse models have also been developed for the examination of healing in more severe long bone critical-size defect injuries, as well

as in articular cartilage injuries that recapitulate osteoarthritic conditions of the limb joints. Therapy is then designed to optimize gene and protein expression and ultimately improve

tissue healing, using cells or growth factors incorporated into novel delivery systems that promote tissue development in severe and chronic health conditions. Fracture repair investigations

are currently directed toward the study of bone repair in tissues compromised by physiological conditions such as obesity and type-2 diabetes, increasingly common in the US population and

among US veterans. The metabolic impairment of the injured tissues will be characterized and tissue metabolism ultimately manipulated to improve conditions for efficient bone repair in these

individuals.  Recent Publications * Rundle CH, GA Gomez, S Pourteymoor, S Mohan (2023) Sequential application of small molecule therapy enhances chondrogenesis and angiogenesis in murine

segmental defect bone repair. J Orthop Res. 41(7): 1471-1481/ doi: 10.1002/jor.25493. * Gomez GA, CH Rundle, W Xing, C Kesavan, S Pourteymoor, RE Lewis, DR Powell, S Mohan (2022) Contrasting

effects of Ksr2, an obesity gene, on trabecular bone volume and bone marrow adiposity. eLife. 11: e82810. doi: 10.7554. * Kaur A, S Mohan, CH Rundle (2020) A segmental defect adaptation of

the mouse closed femur fracture model for the analysis of severely impaired bone healing. Animal Model Exp Med 3(2): 130-139. * Stiffel V, CH Rundle, MH-C Sheng, S Das, KHW Lau (2020) A

mouse noninvasive intraarticular tibial plateau compression loading-induced injury model of posttraumatic osteoarthritis. Calcif Tissue Int 106(2): 158-171. Kaur A, W Xing, S Mohan, CH

Rundle (2019) Changes in ephrin gene expression during bone healing identify a restricted repertoire of ephrins mediating fracture repair. Histochem Cell Biol: 151(1): 43-55.