In addition to supporting the renal structure, RMICs have been demonstrated to play important roles in the maintenance of body fluid homeostasis and normal systemic blood pressure. Animal studies show that chemical ablation of RMICs with BEA leads to systemic hypertension. RMIC cyclooxygenase-2 expression is also suggested to play important roles in renal response to stress, such as sodium loading and water deprivation. To better understand the molecular basis of the physiological roles of RMICs, a Cre-recombinase/ LoxP-based RMIC-specific gene deletion could be a powerful approach to investigate the significance of specific genes in RMICs. Here, we report an inducible RMIC-specific Crerecombinase line under the control of endogenous tenascin-C promoter. Germline transmission of the transgene was obtained from both of these two lines. Genotyping was achieved through PCR of tail DNA. Mice heterozygous for the tenascin-C-CreER2 allele were viable and of normal size without significant developmental or functional abnormalities. To test if the ectopic genes are expressed in the same pattern as endogenous tenascin-C gene, EGFP expression of the mice heterozygous for the tenascin-C-CreER2 allele was examined. Abundant EGFP expression was observed in the inner renal medulla but not in the cortex or outer medulla. The EGFP-positive cells are arranged in rows, a typical morphology of renal medullary AbMole Butylhydroxyanisole interstitial cells. Co-labeling studies showed that the EGFP did not co-localize with renal collecting duct AbMole Clofentezine marker AQP2 or descending thin limb marker AQP1, but co-localized with renal medullary interstitial cell specific COX2. This pattern is consistent with selective expression of EGFP in the renal medullary interstitial cells. No obvious EGFP was observed in other organs or tissues of adult mice examined including the heart, spleen, liver, skin and brain. The tenascin-CCreER2 knockin mouse is therefore able to be utilized for introducing DNA recombination specifically in the renal medullary interstitial cells of the kidney. By inactivating genes of interest or driving ectopic gene expression specifically in renal medullary interstitial cells though inducing LoxP 
based recombination, this mouse line will greatly facilitate our exploration of the physiological roles of renal medullary interstitial cells. Furthermore, as elevated tenascin-C expression is reported to play important roles in pathological conditions such as inflammation, infection and cancer in multiple organs including the kidney, this tenascin-C-CreER2 knockin mouse may also provide a valuable tool. Indeed, studies have demonstrated that some bacteria and viruses are able to mimic the antigenic profile of the thyroid cell membrane, thereby playing an important role in the onset of autoimmune diseases.