Beta cells are organized into islet structures that allow direct contact and communication between neighboring beta cells. This contact and communication is mediated in part by structures call gap junctions that have previously been demonstrated to be important for synchronizing insulin secretion among the beta cells in an islet. During their studies of one of the components of the beta cell gap junctions, these investigators uncovered a role for a molecule called Cx36 in promoting beta cell survival in addition to its role in insulin secretion. They found that when levels of Cx36 in the beta cell were lowered, the beta cells were more sensitive to stresses associated with T1D and died more readily. Conversely, beta cells with increased Cx36 levels were more resistant to the same stresses and could survive insults that killed normal beta cells. This work suggests that therapeutics that increase Cx36 levels could be useful in protecting beta cells in people with T1D.
Klee, P., Allagnat, F., Pontes, H., Cederroth, M., Charollais, A., Caille, D., Britan, A., Haefliger, J. and Meda, P. (2011). Connexins protect mouse pancreatic beta cells against apoptosis. J. Clin. Invest. 121, 4870-4879.
Ramifications for Individuals with Type 1 Diabetes:
This early work describes a previously unknown role for Cx36 and gap junctions in beta cell survival. The results suggest that targeting Cx36 could be a potentially useful strategy for protecting beta cells from destruction in T1D. Further work will be required to further validate Cx36 as a drug target and to identify and optimize molecules or potential drugs to target Cx36.
This work was supported, in part, by a JDRF grant to Dr. Meda.