Postdoctoral Fellow
McGovern Medical School, The University of Texas Health Science Center, Houston, Texas, 2016
Institute of Cytology, Russian Academy of Sciences, Saint-Petersburg, Russia 2014

Areas of Interest

Research Interests

Kidney physiology: Role of TRP and ClC-K channels in physiology of the cortical collecting duct. Calcium signaling, water and electrolyte transport in the distal nephron.  Role of TRPV4 channel in Polycystic Kidney Disease. Role of TRPV4 in potassium homeostasis. TRPC3 channels in volume regulation.

Blood cell physiology: mechanisms of regulation and function of ion channels in the malignant and normal human blood lymphocytes; the role of Transient Receptor Potential Vanilloid 5/6 (TRPV5/TRPV6) in pathophysiology of blood cell malignization.

Hypertension is the major clinically relevant problem commonly stemming from excessive renal salt retention. Substantial basic and clinical studies show that elevated dietary Na+ can increase blood pressure only when accompanied with high Cl. Variations in dietary salt intake regulate transport in the collecting duct (CD) via the Renin-Angiotensin-Aldosterone System  to shape urinary NaCl excretion. CD has capacity to independently reabsorb Na+ and Cl, but the significance of this is still unknown. Principal cells (PCs) perform electrogenic Na+ reabsorption via the epithelial Na+ channel (ENaC). Activity of the basolateral ClC-K2 chloride channel (ClC-Kb in humans, the channel will be referred as ClC-K2/b) mediates transcellular Cl flux in electrically uncoupled intercalated cells (ICs). Classical paradigm is that aldosterone stimulates ENaC and augments K+ secretion in the CD. However, comparable elevations of aldosterone during hyperkalemia and hypovolemia promote kaliuresis with no volume retention and volume retention with no K+ wasting respectively, giving rise to the phenomenon of “aldosterone paradox”. My research focuses on studying the role of ClC-K2/b-mediated Cl flux in the determination of the profile of CD transport.


  • Tomilin V, Mamenko M, Zaika O, Wing CS, and Pochynyuk O. (2019). TRPV4 deletion protects against hypokalemia during systemic K+ deficiency.  AJP-Renal Physiology. 316(5) F948-956.
  • Cherezova A, Tomilin V (co-first author),  Buncha V, Zaika O, Ortiz PA, Mei F, Cheng X, Mamenko M, and  Pochynyuk O.  (2019). Urinary concentrating defect in mice lacking Epac1 or Epac2.  FASEB J. 33 (2), 2156-2170.
  • Mamenko MV, Zaika OL, Tomilin VN,  Jensen VB, Pochynyuk OM.  (2018). Compromised regulation of the collecting duct ENaC activity in mice lacking AT1a. J Cell Physiol.  233(9): 7217-7225.
  • Tomilin VN, Rief GA, Zaika OL, Wallace DP, Pochynyuk OM.  (2018).  Deficient transient receptor potential vanilloid type 4 function contributes to compromised [Ca2+] homeostasis in human autosomal-dominant polycystic kidney disease cells. FASEB J. 32(8):4612-4623.
  • Tomilin VN, Zaika OL, Subramanya OR, Pochynyuk OM. (2018).  Dietary K+ and Cl independently regulate basolateral conductance in principal and intercalated cells of the collecting duct. Pflugers Arch. 470(2): 339-353.
  • Mamenko MV, Boukelmoune N, Tomilin VN, Zaika OL, Jensen VB, O’Neil RG, Pochynyuk OM. (2017).  The renal TRPV4 channel is essential for adaptation to increased dietary potassium. Kidney International. 91(6): 1398-1409.
  • Mistry AC, Wynne BM, Yu L, Tomilin V, Yue Q, Zhou Y, Al-Khalili O, Mallick R, Cai H, Alli AA, Ko B, Mattheyses A, Bao HF, Pochynyuk O, Theilig F, Eaton DC, Hoover RS. (2016).  The Sodium Chloride Cotransporter (NCC) and Epithelial Sodium Channel (ENaC) Associate. Biochemical J. 473(19): 3237-52.
  • Zaika O, Tomilin V, Mamenko M, Bhalla V, Pochynyuk O. (2016).  New perspective of ClC-Kb/2 chloride channel physiology in the distal renal tubule.  Am J Physiology Renal Physiology. 310(10): F923-30.
  • Zaika O, Palygin O, Tomilin V, Mamenko M, Statushenko A, Pochynyuk O. (2016). Insulin and IGF-1 activate Kir4.1/5.1 channels in cortical collecting duct principal cells to control basolateral membrane voltage.  Am J Phys Renal Phys. 310(4): F311-21.
  • Tomilin V, Mamenko M, Zaika O, Pochynyuk O. (2016).  Role of renal TRP channels in physiology and pathology. Seminars in Immunopathology. 38(3): 371-83.
  • Tomilin VN, Cherezova AL, Negulyaev YA, Semenova SB.  (2016). TRPV5/V6 channels mediate Ca2+ influx in Jurkat T cells under the control of extracellular pH.  J Cellular Biochemistry. 117(1):197-206.
  • Hoover RS, Tomilin V, Hanson LN, Pochynyuk O, Ko B. (2015).  PTH Modulation of NCC Activity Regulates TRPV5 Calcium Reabsorption. Am J Phys Renal Phys. 310(2): F144-51.
  • Mamenko M, Dhande I, Tomilin V, Zaika O, Boukelmoune N, Zhu Y, Gonzalez-Garay ML, Pochynyuk O, Doris PA. (2015). Defective Store-Operated Calcium Entry Causes Partial Nephrogenic Diabetes Insipidus.  J Am Society of Nephrology.  27(7): 2035-48.
  • Tomilin VN, Vassilieva IO, Marakhova II, Neguliaev YA, Semenova SB. (2013).  The functional characteristics of TRPV5 and TRPV6 channels in normal and transformed human blood lymphocytes.   Tsitologiia. 55 (5): 300–306.
  • Vassilieva IO, Tomilin VN, Marakhova II, Shatrova AN, Negulyaev YA, Semenova SB. (2013).  Expression of Transient Receptor Potential Vanilloid Channels TRPV5 and TRPV6 in Human Blood Lymphocytes and Jurkat Leukemia T Cells.  J Membrane Biology. Feb; 246(2):131-40.
  • Ilatovskaya DV, Chubinskiy-Nadezhdin VI, Pavlov TS, Shuyskiy LS, Tomilin V, Palygin O, Staruschenko A, Negulyaev YuA.  (2013). Arp2/3 complex inhibitors adversely affect actin cytoskeleton remodeling in the cultured murine kidney collecting duct M-1 cells. Cell and Tissue Research. 354(3):783-92. PMID: 24036843.