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The Kinetics and Mechanism of Niche Filling in Healthy and Cystic Mice
Alex Yashchenko1, Sarah J Miller, Audrey M Cordova
1Department of Internal Medicine, Division of Nephrology, University of Oklahoma Health Campus, Oklahoma City, Oklahoma, 73104, USA.
Background:
Previous data indicate that bone marrow-derived Ly6c hi monocytes can become tissue-resident macrophages (TRM) when the niche is available. However, the balance between monocyte recruitment and TRM self-proliferation during partial depletion is unclear.
Methods:
We investigated the kinetics and mechanism of kidney resident macrophage (KRM) niche filling in healthy mice and in a mouse model of autosomal dominant polycystic kidney disease (ADPKD) after partial depletion with liposomal clodronate.
Results:
Our data indicate that healthy mice efficiently refilled their KRM niche through monocyte-dependent recruitment, engraftment, and differentiation while cystic mice relied preferentially on in situ KRM self-proliferation for niche filling. Further, we found sex-specific differences in niche-filling capacity in cystic mice as female, but not male, mice were unable to completely fill their niche 90 days post-depletion. The inability of cystic female mice to fill the niche following depletion was likely due to their reduced ability to recruit monocytes and convert them into KRM. Phenotypically, delayed KRM niche filling was associated with worsened outcomes including increased cystic index and kidney fibrosis as well as worsened kidney function.
Conclusions:
Collectively, our data demonstrate that sex and disease status impact the kinetics and mechanism of niche filling in the kidney.
