Pediatrics

Pascale H. Lane, M.D.

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ACADEMIC DEGREES:

Medical School	University of Missouri at Kansas City 8/79-5/85
Residency (Pediatrics)	Michael Reese Hospital and Medical Center, Chicago, IL 7/85-6/86 Rush Medical College, Chicago, IL 7/86-6/88
Fellowship (Pediatric Nephrology)	University of Minnesota, Minneapolis, MN 7/88-6/91

 

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Contact Name: Pascale H. Lane
Phone Number: Office: 559-6055; Lab: 559-2479
e-mail: phlane@unmc.edu

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• GRANT SUPPORT (last 3 years):

Clinical Relevance of the ACI Rat
Agency: Nebraska Kidney Association
Funding Period: 7/1/08-6/30/09
Amount of award: $7,500 direct costs
PI: Pascale H. Lane

Pre- and post-pubertal gene expression in response to diabetes
Agency: National Kidney Foundation of Nebraska
Funding Period: 7/1/06-6/30/07
Amount of award: $7,500
PI: Pascale H. Lane

Impact of puberty on the kidney in diabetes
Agency: NIH; NIDDK
Funding period: 8/1/01-4/30/06
Amount of award: $1,647,213 ($225,000 annual direct)
PI: Pascale H. Lane
Status: Funded and in progress

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• PUBLICATIONS (last 3-5 years):

Lane JT, Ford TC, Larson LR, Chambers WA, Lane PH: Acute Effects of Different Intensities of Exercise in Normoalbuminuric / Normotensive Patients with Type 1 Diabetes Mellitus. Diabetes Care 27:28-32, 2004

McCurdy FA, Beck G, Maroon A, Gomes H, Lane PH: The Administrative Colloquium: Developing management and leadership skills for faculty. Ambul Pediatr 4:124-8, 2004

Lovegrove AS, Sun J, Gould KA, Lubahn DB, Korach KS, Lane PH: Estrogen receptor α mediated events promote sex-specific diabetic glomerular hypertrophy. Am J Physiol Renal Physiol 287:F586-F591, 2004

Lane PH, Sun J, Devish K, Langer WJ: Dissociation of renal TGF-β and hypertrophy in female rats with diabetes mellitus. Am J Physiol Renal Physiol 287:F1011-F1020, 2004

Wei P, Lane PH, Lane JT, Padanilam B, Sansom SC: Mesangial expansion precedes hyperfiltration in a mouse model of insulin resistance syndrome. Diabetologia 47:1541-1549, 2004

Sun J, Langer WJ, Devish K, Lane PH: Compensatory kidney growth in estrogen receptor α null mice. Am J Physiol Renal Physiol 290:F319-F323, 2006

Sun J, Devish K, Langer WJ, Carmines PK, Lane PH: Testosterone treatment promotes tubular damage in experimental diabetes in pre-pubertal rats. Am J Physiol Renal Physiol 292:F1681-1690, 2007

Lane JT, Ferguson A, Hall J, McElligott M, Miller M, Lane PH, Pfeffer E: Glycemic Control Over 3 Years In A Young Adult Clinic For Patients With Type 1 Diabetes. Diabetes Res Clin Pract 78:385-391, 2007

Langer WJ, Devish K, Carmines PK, Lane PH: Prepubertal onset of diabetes prevents renal cortical connective tissue growth factor expression. Pediatr Nephrol 23:275-283, 2008

Bynote KK, Hackenberg JM, Korach KS, Lubahn DB, Lane PH, Gould KA: Estrogen receptor alpha deficiency attenuates autoimmune disease in (NZB xNZW) F1 mice. Genes Immun 9:137-152, 2008

Troncoso Brindeiro CM, Fallet RW, Lane PH, Carmines PK Potassium channel contributions to afferent arteriolar tone in normal and diabetic rat kidney. Am J Physiol Renal Physiol 295:F171-F178, 2008

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• PREVIOUS GRADUATE STUDENTS/POST-DOCTORAL FELLOWS (present location):

None

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• CURRENT RESEARCH PROJECTS:

Impact of Puberty on the Kidney in Diabetes
The prepubertal years of type 1 diabetes (DM) appear to be protected from expression of nephropathy and other microvascular complications. Puberty also seems to accelerate other kidney disorders. Preliminary data from our laboratory suggests that connective tissue growth factor (CTGF) expression may not occur in response to DM until puberty, perhaps explaining the increased susceptibility to progression. Ongoing experiments attempt to identify the mechanism(s) through which CTGF transcription is permitted after sexual maturity.
 

Estrogen receptors alpha and beta in diabetic glomerulopathy
Estrogen (E) may provide protection in progressive kidney disorders, including diabetes (DM).  E blocks pro-sclerotic effects in mesangial cells in vitro, and these cells express both estrogen receptors a and b (ERa, ERb). Dysregulation of E and ER occurs in patients and animals with DM.  Mice lacking ERa (aERKO) are protected from glomerular hypertrophy, an early marker of DM glomerulopathy, while ovariectomized rats have no protection. The major difference between aERKO mice and ovariectomized rats is aERKO mice have increased stimulation of ERb, while ovariectomy suppresses both ERa- and ERb-mediated processes, suggesting that ERb-mediated events may protect aERKO mice from DM glomerular hypertrophy. Overall hypothesis: ERb-mediated processes are protective and ERα-mediated processes are detrimental in diabetic glomerulopathy in females.
Specific Aims: 1)Characterize kidney structure and function through 12 weeks of diabetes in wild-type and aERKO female mice; 2)Characterize kidney structure and function through 12 weeks of diabetes in wild-type and bERKO female mice; 3)Characterize kidney structure and function through 12 weeks of diabetes in wild-type and abERKO female mice; and 4)Identify processes that respond differently to ERa and ERb in mesangial cells.
Methods: Wild-type and ERKO female mice with streptozocin DM will be studied with telemetric blood pressure, glomerular filtration rate, albuminuria, renal morphometric studies, immunohistochemistry, and blood hormone levels. Proteins and mRNA of interest will be measured in whole kidney and isolated glomeruli. Experiments will include intact and ovariectomized animals with and without hormone or anti-estrogen treatments. Primary cultures of mesangial cells from wild-type and ERKO mice exposed to normal and high glucose media, with or without estrogen or anti-estrogen, will be used to explore mitogen-activated protein kinases ERK1/2 and p38 as a candidate system interacting in these processes.
Health Implications: With knowledge of ER-specific effects, selective estrogen receptor modulators beneficial to the kidney without adverse effects might be developed, rapidly resulting in new treatments for diabetic kidney disease, the most important cause of kidney failure in the US.

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• SPECIALIZED LABORATORY/CLINICAL RESEARCH RESOURCES:

ELISA for all isoforms of TGF-; digital color image analysis;whole-mouse physiology.

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