Subspecialty	Pediatric Nephrology
Clinical Interests	Pediatrics
	Electrolyte Disorders
	Hypertension
Languages	English
	French
	Spanish
Gender	Female
E-mail	lisa.satlin@mssm.edu
Education and Training	MD, Columbia Univ. Col. of Phy. & Surg.
	Residency, Pediatrics, Columbia-Presbyterian Medical Ctr.
	Fellowship, Nephrology, Albert Einstein College of Medicine
Awards	2009 Best Doctors New York Magazine

Curriculum Vitae: http://www.mountsinai.org/supporting-files/cv/satl...

Education and Training	MD, Columbia Univ. Col. of Phy. & Surg.
	Residency, Pediatrics, Columbia-Presbyterian Medical Ctr.
	Fellowship, Nephrology, Albert Einstein College of Medicine
Board Certification	Pediatric Nephrology

Subspecialty	Pediatric Nephrology
Clinical Interests	Pediatrics
	Electrolyte Disorders
	Hypertension
Languages	English
	French
	Spanish
Board Certification	Pediatric Nephrology

The focus of our lab is directed at defining the mechanisms leading to the acquisition, maintenance and regulation of transepithelial transport in the renal cortical collecting duct (CCD), the nephron segment responsible in the adult for the final renal regulation of potassium (K) and sodium (Na) homeostasis. In the CCD, urinary Na diffuses into principal cells through apical Na channels (ENaCs) and is extruded at the basolateral membrane in exchange for uptake of K by the Na-K pump. Cell K passively diffuses out of the cell down a favorable electrochemical gradient into the luminal fluid through apical K-selective (SK or ROMK) channels. Recent evidence from our laboratory indicates that high rates of tubular fluid flow activate apical maxi-K channels in a Ca2+-dependent manner. Using a combination of molecular, electrophysiologic, and functional techniques, we are exploring following two major areas of investigation.

Developmental regulation of ion channels in the distal nephron: Kidneys of growing subjects efficiently retain urinary K and Na. In contrast to the high rates of net K secretion observed in CCDs isolated from adult animals, segments from neonatal animals show no K transport and a paucity of conducting apical K channels. Yet, the same neonatal segments possess functional ENaC channels and absorb Na at a rate half that measured in the adult. Studies are underway to discern whether the appearance of conducting SK, maxi-K, and ENaC channels is regulated by transcription, translation, and/or post-translational processing. The role of epigenetic factors (diet and hormones) and signaling molecules in the regulation of gene and protein expression, channel activity, and tubular transport in the differentiating CCD are being explored.

Epithelial transport in polycystic kidney disease (PKD): Autosomal recessive PKD (ARPKD), a disease associated with a high morbidity, is characterized by the progressive dilatation of CCDs and early onset of hypertension. We have sought to identify whether alterations in expression and regulation of epithelial cell transport pathways contribute to disease progression. Preliminary data indicates that cyst-lining cells are capable of avid Na absorption and maintaining steep transepithelial ion gradients. Studies are ongoing to examine the molecular basis for this observation, specifically focusing on exploring the impact of mispolarized EGFR on activity of the major channel, transporter, and receptor proteins involved in solute and water transport in kidney cell lines derived from ARPKD and age-matched normal kidneys.

Sun P, Liu W, Lin DH, Yue P, Kemp R, Satlin LM, Wang WH. Epoxyeicosatrienoic acid activates BK channels in the cortical collecting duct. J. Am. Soc. Nephrol 2009; 20: 513-520.

Estilo G, Liu W, Pastor-Soler N, Mitchell P, Kleyman T, Satlin LM. Effect of mineralocorticoids on maxi-K channel expression in the cortical collecting duct (CCD). Am. J. Physiol. Renal Physiol 2008; 295: F780-F788.

Rohatgi R, Battini L, Kim P, Israel S, Wilson PD, Gusella GL, Satlin LM. Mechanoregulation of intracellular Ca2+ in human autosomal recessive polycystic kidney disease (ARPKD) cyst-lining renal epithelial cells. Am J Physiol Renal Physiol 2008; 294: F890-F899.

Carattino MD, Liu W, Hill W, Satlin LM, Kleyman TR. Lack of a role of membrane-protein interactions in flow-dependent activation of ENaC. American Journal of Physiology - Renal Physiology 2007; 293: F316-F324.

Liu W, Morimoto T, Woda C, Kleyman TR, Satlin LM. Ca2-dependence of flow-stimulation of K secretion in the mammalian collecting duct. American Journal of Physiology - Renal Physiology 2007; 293: F227-F235.

Wei Y, Zavilowitz B, Satlin LM, Wang W. Angiotensin II inhabits the ROMK-like small conductance K channel in renal cortical collecting duct during dietary potassium restriction. J Biol Chem 2007; 282: 6455-6462.

Satlin LM, Carattino M, Liu W, Kleyman TR. Regulation of cation transport in the distal nephron by mechanical forces. American Journal of Physiolocy 2006; 291: F923-F931.

Morimoto T, Liu W, Woda C, Carattino MS, Wei Y, Hughey RP, Apodaca G, Satlin* LM, Kleyman TR. Mechanism underlying flow-stimulation of Na absorption in the mammalian collecting duct (* corresponding author). American Journal of Physiology 2006; 291: F663-F669.

Najjar F, Zhou H, Morimoto T, Satlin LM, Li HS, Liu W, Kleyman TR, Bruns JB. Dietary K+ regulates apical membrane expression of maxi-K channels in rabbit cortical collecting dust. American Journal of Physiology - Renal Physiology 2005; 289: 922-932.