Abstract
Aquaporin-2–4 (AQP) are expressed in the principal cells of the renal collecting duct (CD). Beside their role in water transport across membranes, several studies showed that AQPs can influence the migration of cells. It is unknown whether this also applies for renal CD cells. Another fact is that the expression of these AQPs is highly modulated by the external osmolality. Here we analyzed the localization of AQP2–4 in primary cultured renal inner medullary CD (IMCD) cells and how osmolality influences the migration behavior of these cells. The primary IMCD cells showed a collective migration behavior and there were no differences in the migration speed between cells cultivated either at 300 or 600 mosmol/kg. Acute increase from 300 to 600 mosmol/kg led to a marked reduction and vice versa an acute decrease from 600 to 300 mosmol/kg to a marked increase in migration speed. Interestingly, none of the analyzed AQPs were localized at the leading edge. While AQP3 disappeared within the first 2–3 rows of cells, AQP4 was enriched at the rear end. Further analysis indicated that migration induced lysosomal degradation of AQP3. This could be prevented by activation of the protein kinase A, inducing localization of AQP3 and AQP2 at the leading edge and increasing the migration speed.
Highlights
Aquaporin-2–4 (AQP) are expressed in the principal cells of the renal collecting duct (CD)
We have recently shown that hyper osmolality induces the expression of AQP2 and the expression of other major principal cell markers like AQP3-4, the urea transporter Slc14a1 or vasopressin type 2 receptor m RNAs19
The results showed that the protein expression of AQP3 and AQP4 was increased 26- and 5-fold, respectively, in inner medullary collecting duct (IMCD) cells cultivated at 600 mosmol/kg compared with those cultivated at 300 mosmol/kg
Summary
Aquaporin-2–4 (AQP) are expressed in the principal cells of the renal collecting duct (CD). Beside their role in water transport across membranes, several studies showed that AQPs can influence the migration of cells. It is unknown whether this applies for renal CD cells. Water transport during cell migration was proposed as a major mechanism already 25 years ago with local cell swelling and shrinkage occurring at the cell front and rear end, r espectively[25]. Water flow across the plasma membrane of the leading edge provides an additional protrusive force[27]
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