George I. Gorodeski

Case Western Reserve University

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Wulf H. Utian

Intelligent Mechatronic Systems (United States)

Ellen A. Rorke

University of Maryland, Baltimore

Ulrich Hopfer

Case Western Reserve University

Richard L. Eckert

Case Western Reserve University

Fadi W. Abdul‐Karim

Cleveland Clinic

J. Goldfarb

University Hospitals of Cleveland

Xiaoping Qi

University of Alabama at Birmingham

Ying‐Hong Feng

Sun Yat-sen University

Lingyin Zhou

Case Western Reserve University

Robin Zeng

Dartmouth Hospital

Cooperative Institutions

Case Western Reserve University

University School

Columbia University

Weatherford College

University Hospitals of Cleveland

Brigham and Women's Hospital

Columbia University Irving Medical Center

University of Southern California

Harvard University

University of California, San Diego

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Endogenously Expressed Truncated P2X7 Receptor Lacking the C-Terminus is Preferentially Upregulated in Epithelial Cancer Cells and Fails to Mediate Ligand-Induced Pore Formation and Apoptosis

Nucleosides Nucleotides & Nucleic Acids (2006)

Ying Feng Xinrui Li Robin Zeng George I. Gorodeski

A truncated naturally occurring variant of the human purinergic receptor P2X7 (P2X7-R) was found in human cancer cervical cells. The novel protein consists of 258 amino acids, and compared to the wild-type P2X7-R it lacks the entire intracellular carboxy terminus, the second transmembrane domain, and the distal third of the extracellular loop. The truncated P2X7-R failed to form pores and mediate apoptosis, and it interacted with the wild-type P2X7-R in a manner suggesting auto-hetero-oligomerization. In contrast to cancer cells the novel truncated P2X7-R was expressed relatively little in normal cervical cells. These data raise the possibility that coexpression of the truncated form could block P2X7 mediated apoptosis and promote uncontrolled growth of cells.

HEK 293 cells

10.1080/15257770600890921

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Citations (37)

Osmolar changes regulate the paracellular permeability of cultured human cervical epithelium

AJP Cell Physiology (1995)

George I. Gorodeski B. J. De Santis J. Goldfarb Wulf H. Utian Ulrich Hopfer

Extracellular nucleotides induce a biphasic change in the transepithelial electrical conductance (GT) of human cervical cells grown on filters: a rapid increase (phase I) followed by a sustained decrease (phase II). To probe the involvement of the intercellular space, its magnitude was varied by manipulating cell volume through changes in extracellular osmolarity. Under baseline conditions [GT = 115 mS/cm2 (approximately 9 omega.cm2)] and during phase II, hypertonic challenges resulted in an increase in GT (0.98% .mosmol-1.l-1 and 0.73%.mosmol-1.l-1, respectively). However, a hypertonic challenge during phase I decreased GT (-0.16%.mosmol-1.l-1). Hypotonic challenges decreased GT during baseline, phase I, and phase II conditions by -1%.mosmol-1.l-1. Similar trends were observed with regard to pyranine permeability. Reduction of extracellular calcium increased GT, abrogated the phase II effect of extracellular ATP, and reversed the effect of a hypertonic challenge. The additive nature of the permeability changes in response to osmotic challenges and to ATP during phase II suggests that different sites are involved in each response, i.e., the resistance of the intercellular space changes with osmolarity and that of the tight junction during phase II.

Osmotic concentration

Paracellular transport

10.1152/ajpcell.1995.269.4.c870

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Citations (40)

Free Communication

Menopause The Journal of The North American Menopause Society (1994)

George I. Gorodeski Wulf H. Utian Miles Levy

Departments of Reproductive Biology and *Physiology and Biophysics, Case Western Reserve School of Medicine; and *Division of Investigative Medicine, Mt. Sinai Medical Center, Cleveland, Ohio, U.S.A.

10.1097/00042192-199400130-00010

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Citations (1)

Estrogen Attenuates P2X₇‐R—Mediated Apoptosis of Uterine Cervical Cells by Blocking Calcium Influx

Nucleosides Nucleotides & Nucleic Acids (2004)

George I. Gorodeski

Estrogen blocks apoptosis of human ectocervical epithelial cells by modulating P2X7/Ca2+ influx. The effect involves decreased Ca2+-influx and cytosolic-calcium-increase via ATP-activated P2X7 pores. This mechanism may have physiological significance in the human cervix, in-vivo, and the results suggest a physiological role for estrogen in the cervix as an anti-apoptotic factor.

10.1081/ncn-200027549

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Citations (17)

Estrogen modulation of epithelial permeability in cervical-vaginal cells of premenopausal and postmenopausal women

Menopause The Journal of The North American Menopause Society (2007)

George I. Gorodeski

In Brief Objective: To understand how menopause affects estrogen regulation of epithelial permeability. Design: Experimental study using human normal epithelial vaginal-ectocervical cells obtained from premenopausal and postmenopausal women. Endpoints were paracellular permeability (determined in terms of the resistance of the lateral intercellular space [RLIS] and tight junctions [RTJ]); cellular G-actin; nonmuscle myosin type II-B (NMMII-B) filamentation and magnesium-adenosine triphosphatase activity; and occludin expression (in terms of expression of the functional 65-kd and truncated 50-kd forms). Results: Estrogen induced an early transient decrease in RLIS that correlated in time with increases in cellular G-actin and NMMII-B magnesium-adenosine triphosphatase activity and with decreases in NMMII-B filamentation and a slower decrease in RTJ that correlated with up-regulation of the 50-kd form of occludin. Estrogen modulation of G-actin NMMII-B and occludin could be described in terms of interaction with the estrogen receptor mechanism. The potency of estrogen effects was similar in cells of premenopausal and postmenopausal women, but the effects occurred earlier in cells of premenopausal women. RLIS returned to baseline faster in cells of postmenopausal women, and the effect was associated with faster reversal of estrogen changes in NMMII-B despite the continued presence of estrogen in the culture medium, suggesting that desensitization of the actin-myosin effects to estrogen actions occur distal to the estrogen receptor. Conclusions: The results suggest that the transient estrogen decrease in RLIS is mediated by modulation of actomyosin, and it is affected by the aging process. In contrast, the late persistent decrease in RTJ is mediated by occludin degradation and is unrelated to aging. The objective of the study was to understand how menopause affects estrogen regulation of epithelial permeability through modulation of the paracellular resistance (ie, the resistance of the lateral intercellular space and the tight junctional resistance). The results suggest that the estrogen transient decrease in the resistance of the lateral intercellular space is mediated by modulation of the actomyosin and is affected by occludin degradation and is unrelated to aging.

10.1097/gme.0b013e3180587eb5

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Citations (41)

Sex hormone modulation of flow velocity in the parametrial artery of the pregnant rat

AJP Regulatory Integrative and Comparative Physiology (1995)

George I. Gorodeski Leon A. Sheean Wulf H. Utian

The objective of the study was to correlate the disparate distal/proximal state of maturation of uterine segments in the rat with the hemodynamics of the parametrial uterine artery. Flow velocity was determined by the methylene blue photometric analysis. In nonpregnant animals, the velocity in the distal (VD-->P) and proximal (VP-->D) portions of the parametrial artery were similar, but in late pregnancy, VD-->P was higher than VP-->D. The difference was associated with an increased width of the distal part of the parametrial artery. In addition, the distance from the proximal end of the parametrial artery where the D-->P and P-->D streams collided decreased in animals in late pregnancy, compared with nonpregnant animals. Treatment with estradiol and RU-486 reversed the pregnancy-related hemodynamic changes. The pregnancy-related shift in flow velocity in the parametrial artery is crucial to rat fetal survival in utero and may be a mechanism in vivo for promoting maturation of distal, compared with proximal, segments of the uterine horn.

Parametrial

Uterine horns

10.1152/ajpregu.1995.268.3.r614

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Citations (14)

Is progesterone a vasodilator?

Menopause The Journal of The North American Menopause Society (2004)

George I. Gorodeski

Departments of Reproductive Biology, Oncology, and Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio

Vasodilator agents

10.1097/01.gme.0000123644.01891.36

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Citations (0)

A novel fluorescence chamber for the determination of volume changes in human CaSki cell cultures attached on filters

Cell Biochemistry and Biophysics (1998)

George I. Gorodeski J. Whittembury

Ionomycin

BAPTA

Nigericin

Ussing chamber

Osmotic concentration

10.1007/bf02737900

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Citations (21)

Retinoids modulate P_2Upurinergic receptor-mediated changes in transcervical paracellular permeability

AJP Cell Physiology (1998)

George I. Gorodeski Dipika Pal Ellen A. Rorke Richard L. Eckert Peter Burfeind

In human cervical cells, extracellular ATP induces an acute decrease in the resistance of the lateral intercellular space, the phase I response, followed by a delayed increase in tight junctional resistance, the phase II response. These responses depend on vitamin A because incubation of cells in retinoid-free medium (RFM) abolished both responses. Treatment with retinoic acid restored the phase I response in full, but the amplitude of the phase II response was restored only partly. Shorter incubations and lower concentrations of retinoic acid [half-maximal effective concentration ( K ½ ) = 0.1 μM] were required for restoring the phase I response than were required for reversing the phase II response ( K ½ = 1 μM). The phase I response could be restored by ligands that bind to either retinoic acid receptors (RARs) or retinoid X receptors, but only RAR agonists had an effect on phase II response. RFM had no effect on decreases in resistance induced by ionomycin, but it attenuated phase II-like increases in resistance induced by KCl or by 1,2-dioctanoyl- sn-diglycerol (diC8). Actinomycin D blocked phase IIresponse but not phase I response or the responses to ionomycin, KCl, or diC8. These results suggest that retinoids act on cervical cells via distinct retinoid receptor mechanisms and modulate phase I and phase II changes in resistance by regulating distinct signal mechanisms.

Ionomycin

10.1152/ajpcell.1998.274.4.c1108

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Citations (7)

George I. Gorodeski, MD, PhD: 2005-2006 NAMS President

Menopause The Journal of The North American Menopause Society (2005)

George I. Gorodeski

Professor of Reproductive Biology, Oncology, and Physiology and Biophysics at Case Western Reserve University School of Medicine, and a full-time faculty member in the Department of Obstetrics and Gynecology of University MacDonald Women's Hospital, University Hospitals of Cleveland, both in Cleveland, OH. George I. Gorodeski, MD, PhD, has been elected President of The North American Menopause Society (NAMS) for the 2005-2006 term. The election took place during the 16th Annual NAMS Meeting in San Diego, CA, held September 28 to October 1, 2005.

George (robot)

10.1097/01.gme.0000187662.57082.41

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Citations (2)