Hai, Chi-Ming

Chi-Ming Hai

Professor Emeritus of Molecular Pharmacology, Physiology and Biotechnology

Overview

Chi-Ming Hai, Ph.D. graduated from the University of Toronto with a B.S. in Physiology in 1978. He continued his studies in Physiology at the School of Medicine at the University of Ottawa, receiving his M.S. degree in 1980. He then proceeded to the School of Medicine at Johns Hopkins University in Maryland where he graduated with his Ph.D. in Physiology in 1984. Dr. Hai has been teaching at Brown University since 1988.

Brown Affiliations

Molecular Pharmacology, Physiology and Biotechnology

Research Areas

Publications Visualize it

Gu Z, Fonseca V, Hai CM. "Nicotinic acetylcholine receptor mediates nicotine-induced actin cytoskeletal remodeling and extracellular matrix degradation by vascular smooth muscle cells." Vascular pharmacology, vol. 58, no. 1-2, 2013, pp. 87-97.

Full Text PubMed

Hai, Chi-Ming. "Cigarette Smoke and Nicotine-Induced Remodeling of Actin Cytoskeleton and Extracellular Matrix by Vascular Smooth Muscle Cells." Biophysical Journal, vol. 102, no. 3, 2012, pp. 118a.

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Hai CM. "Editorial: novel technologies for developing clinically useful hemoglobin-based oxygen carriers." Current drug discovery technologies, vol. 9, no. 3, 2012, pp. 157.

Full Text PubMed

Hai CM. "Systems biology of HBOC-induced vasoconstriction." Current drug discovery technologies, vol. 9, no. 3, 2012, pp. 204-11.

Full Text PubMed

Wu Z, Aron AW, Macksoud EE, Iozzo RV, Hai CM, Lechner BE. "Uterine dysfunction in biglycan and decorin deficient mice leads to dystocia during parturition." PLoS ONE, vol. 7, no. 1, 2012, pp. e29627.

Full Text PubMed

Kim HR, Liu K, Roberts TJ, Hai CM. "Length-dependent modulation of cytoskeletal remodeling and mechanical energetics in airway smooth muscle." American Journal of Respiratory Cell and Molecular Biology, vol. 44, no. 6, 2011, pp. 888-97.

Full Text PubMed

Fonseca V, Avizinis J, Moon-Massat P, Freilich D, Kim HW, Hai CM. "Differential sensitivities of pulmonary and coronary arteries to hemoglobin-based oxygen carriers and nitrovasodilators: study in a bovine ex vivo model of vascular strips." Vascular pharmacology, vol. 52, no. 5-6, 2010, pp. 215-23.

Full Text PubMed

Kim HW, Hai CM, Greenburg AG. "Relative roles of heme-irons and globin-thiols in the genesis of acellular hemoglobin mediated vasoconstriction." Artificial cells, blood substitutes, and immobilization biotechnology, vol. 38, no. 1, 2010, pp. 5-12.

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Hai CM. "Caldesmon as a therapeutic target for proliferative vascular diseases." Mini reviews in medicinal chemistry, vol. 8, no. 12, 2008, pp. 1209-13.

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Hai CM. "Mechanistic systems biology of inflammatory gene expression in airway smooth muscle as tool for asthma drug development." Current drug discovery technologies, vol. 5, no. 4, 2008, pp. 279-88.

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Hai CM. "Airway smooth muscle cell as therapeutic target of inflammation." Current medicinal chemistry, vol. 14, no. 1, 2007, pp. 67-76.

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Gu Z, Kordowska J, Williams GL, Wang CL, Hai CM. "Erk1/2 MAPK and caldesmon differentially regulate podosome dynamics in A7r5 vascular smooth muscle cells." Experimental Cell Research, vol. 313, no. 5, 2007, pp. 849-66.

Full Text PubMed

Hai CM, Gu Z. "Caldesmon phosphorylation in actin cytoskeletal remodeling." European journal of cell biology, vol. 85, no. 3-4, 2006, pp. 305-9.

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Kanefsky J, Lenburg M, Hai CM. "Cholinergic receptor and cyclic stretch-mediated inflammatory gene expression in intact ASM." American Journal of Respiratory Cell and Molecular Biology, vol. 34, no. 4, 2006, pp. 417-25.

Full Text PubMed

Hai CM, Kim HR. "An expanded latch-bridge model of protein kinase C-mediated smooth muscle contraction." Journal of Applied Physiology, vol. 98, no. 4, 2005, pp. 1356-65.

Full Text PubMed

Kim HR, Hai CM. "Mechanisms of mechanical strain memory in airway smooth muscle." Canadian journal of physiology and pharmacology, vol. 83, no. 10, 2005, pp. 811-5.

Full Text PubMed

Kim HR, Hoque M, Hai CM. "Cholinergic receptor-mediated differential cytoskeletal recruitment of actin- and integrin-binding proteins in intact airway smooth muscle." AJP: Cell Physiology, vol. 287, no. 5, 2004, pp. C1375-83.

Full Text PubMed

Lu Q, Harrington EO, Hai CM, Newton J, Garber M, Hirase T, Rounds S. "Isoprenylcysteine carboxyl methyltransferase modulates endothelial monolayer permeability: involvement of RhoA carboxyl methylation." Circulation research, vol. 94, no. 3, 2004, pp. 306-15.

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Bai TR, Bates JH, Brusasco V, Camoretti-Mercado B, Chitano P, Deng LH, Dowell M, Fabry B, Ford LE, Fredberg JJ, Gerthoffer WT, Gilbert SH, Gunst SJ, Hai CM, Halayko AJ, Hirst SJ, James AL, Janssen LJ, Jones KA, King GG, Lakser OJ, Lambert RK, Lauzon AM, Lutchen KR, Maksym GN, Meiss RA, Mijailovich SM, Mitchell HW, Mitchell RW, Mitzner W, Murphy TM, Paré PD, Schellenberg RR, Seow CY, Sieck GC, Smith PG, Smolensky AV, Solway J, Stephens NL, Stewart AG, Tang DD, Wang L. "On the terminology for describing the length-force relationship and its changes in airway smooth muscle." Journal of Applied Physiology, vol. 97, no. 6, 2004, pp. 2029-34.

Full Text PubMed

Wahl M, Eddinger TJ, Hai CM. "Sinusoidal length oscillation- and receptor-mediated mRNA expression of myosin isoforms and alpha-SM actin in airway smooth muscle." AJP: Cell Physiology, vol. 287, no. 6, 2004, pp. C1697-708.

Full Text PubMed

Hai CM, Hahne P, Harrington EO, Gimona M. "Conventional protein kinase C mediates phorbol-dibutyrate-induced cytoskeletal remodeling in a7r5 smooth muscle cells." Experimental Cell Research, vol. 280, no. 1, 2002, pp. 64-74.

Full Text PubMed

Silberstein J, Hai CM. "Dynamics of length-force relations in airway smooth muscle." Respiratory physiology & neurobiology, vol. 132, no. 2, 2002, pp. 205-21.

Full Text PubMed

Hai CM, Sadowska G, Francois L, Stonestreet BS. "Maternal dexamethasone treatment alters myosin isoform expression and contractile dynamics in fetal arteries." AJP: Heart and Circulatory Physiology, vol. 283, no. 5, 2002, pp. H1743-9.

Full Text PubMed

An SS, Hai CM. "Mechanical signals and mechanosensitive modulation of intracellular [Ca(2+)] in smooth muscle." AJP: Cell Physiology, vol. 279, no. 5, 2000, pp. C1375-84.

Full Text PubMed

Chan WL, Silberstein J, Hai CM. "Mechanical strain memory in airway smooth muscle." AJP: Cell Physiology, vol. 278, no. 5, 2000, pp. C895-904.

Full Text PubMed

Hai CM. "Mechanosensitive modulation of receptor-mediated crossbridge activation and cytoskeletal organization in airway smooth muscle." Archives of pharmacal research, vol. 23, no. 6, 2000, pp. 535-47.

Full Text PubMed

An SS, Hai CM. "Mechanical strain modulates maximal phosphatidylinositol turnover in airway smooth muscle." The American journal of physiology, vol. 277, no. 5 Pt 1, 1999, pp. L968-74.

PubMed

An SS, Hai CM. "Mechanical strain modulates maximal phosphatidylinositol turnover in airway smooth muscle." American Journal of Physiology-Lung Cellular and Molecular Physiology, vol. 277, no. 5, 1999, pp. L968-L974.

Full Text PubMed

Wong CT, Hai CM. "Mucosal modulation of agonist-induced myosin phosphorylation and contraction in airway smooth muscle." Respiration physiology, vol. 115, no. 1, 1999, pp. 103-11.

Full Text PubMed

Youn T, Kim SA, Hai CM. "Length-dependent modulation of smooth muscle activation: effects of agonist, cytochalasin, and temperature." The American journal of physiology, vol. 274, no. 6 Pt 1, 1998, pp. C1601-7.

PubMed

Youn T, Kim SA, Hai CM. "Length-dependent modulation of smooth muscle activation: effects of agonist, cytochalasin, and temperature." AJP: Cell Physiology, vol. 274, no. 6, 1998, pp. C1601-C1607.

Full Text PubMed

Tseng S, Kim R, Kim T, Morgan KG, Hai CM. "F-actin disruption attenuates agonist-induced [Ca2+], myosin phosphorylation, and force in smooth muscle." The American journal of physiology, vol. 272, no. 6 Pt 1, 1997, pp. C1960-7.

PubMed

Szeto B, Hai CM. "Length-dependent modulation of myosin phosphorylation and contractile force in coronary arterial smooth muscle." Archives of Biochemistry and Biophysics, vol. 329, no. 2, 1996, pp. 241-8.

Full Text PubMed

Yoo J, Ellis R, Morgan KG, Hai CM. "Mechanosensitive modulation of myosin phosphorylation and phosphatidylinositol turnover in smooth muscle." The American journal of physiology, vol. 267, no. 6 Pt 1, 1994, pp. C1657-65.

PubMed

Hai CM, Watson C, Wallach SJ, Reyes V, Kim E, Xu J. "Effects of substrate and inhibition of oxidative metabolism on contraction and myosin phosphorylation in ASM." The American journal of physiology, vol. 264, no. 6 Pt 1, 1993, pp. L553-9.

PubMed

Hai CM, Ma CB. "Fluoroaluminate- and GTP gamma S-induced stress, shortening, and myosin phosphorylation in airway smooth muscle." The American journal of physiology, vol. 265, no. 1 Pt 1, 1993, pp. L73-9.

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Hai CM, Karlin N. "Time-dependent uncoupling between myosin phosphorylation and contractile force induced by Ca(2+)-depletion in smooth muscle." Archives of Biochemistry and Biophysics, vol. 301, no. 2, 1993, pp. 299-304.

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Hai CM, Murphy RA. "Adenosine 5'-triphosphate consumption by smooth muscle as predicted by the coupled four-state crossbridge model." Biophysical Journal, vol. 61, no. 2, 1992, pp. 530-41.

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Hai CM, Szeto B. "Agonist-induced myosin phosphorylation during isometric contraction and unloaded shortening in airway smooth muscle." The American journal of physiology, vol. 262, no. 1 Pt 1, 1992, pp. L53-62.

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Hai CM, Rembold CM, Murphy RA. "Can different four-state crossbridge models explain latch and the energetics of vascular smooth muscle?." Systems Biology of RNA Binding Proteins, vol. 304, 1991, pp. 159-70.

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Hai CM. "Length-dependent myosin phosphorylation and contraction of arterial smooth muscle." Pflugers Archiv : European journal of physiology, vol. 418, no. 6, 1991, pp. 564-71.

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Murphy RA, Rembold CM, Hai CM. "Contraction in smooth muscle: what is latch?." Progress in clinical and biological research, vol. 327, 1990, pp. 39-50.

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Hai CM, Murphy RA. "Crossbridge phosphorylation and regulation of vascular smooth muscle contraction." American Journal of Hypertension, vol. 3, no. 8 Pt 2, 1990, pp. 235S-237S.

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Hai CM, Murphy RA. "Ca2+, crossbridge phosphorylation, and contraction." Annual review of physiology, vol. 51, 1989, pp. 285-98.

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Hai CM, Murphy RA. "Cross-bridge dephosphorylation and relaxation of vascular smooth muscle." The American journal of physiology, vol. 256, no. 2 Pt 1, 1989, pp. C282-7.

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Hai CM, Murphy RA. "Crossbridge phosphorylation and the energetics of contraction in the swine carotid media." Progress in clinical and biological research, vol. 315, 1989, pp. 253-63.

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Ratz PH, Hai CM, Murphy RA. "Dependence of stress on cross-bridge phosphorylation in vascular smooth muscle." The American journal of physiology, vol. 256, no. 1 Pt 1, 1989, pp. C96-100.

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Hai CM, Phair RD. "Forskolin and caffeine induce Ca2+ release from intracellular stores in rabbit aorta." The American journal of physiology, vol. 257, no. 3 Pt 1, 1989, pp. C413-8.

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Hai CM, Murphy RA. "Cross-bridge phosphorylation and regulation of latch state in smooth muscle." The American journal of physiology, vol. 254, no. 1 Pt 1, 1988, pp. C99-106.

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Hai CM, Murphy RA. "Regulation of shortening velocity by cross-bridge phosphorylation in smooth muscle." The American journal of physiology, vol. 255, no. 1 Pt 1, 1988, pp. C86-94.

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Hai CM, Murphy RA. "Sr2+ activates cross-bridge phosphorylation and latch state in smooth muscle." The American journal of physiology, vol. 255, no. 3 Pt 1, 1988, pp. C401-7.

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Hai CM, Murphy RA. "Ba2+ induces contraction in swine carotid artery by mobilizing intracellular Ca2+." The American journal of physiology, vol. 252, no. 4 Pt 1, 1987, pp. C378-84.

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Chatterjee M, Hai CM, Murphy RA. "Dependence of stress and velocity on Ca2+ and myosin phosphorylation in the skinned swine carotid media." Progress in clinical and biological research, vol. 245, 1987, pp. 399-410.

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Murphy RA, Ratz PH, Hai CM. "Determinants of the latch state in vascular smooth muscle." Progress in clinical and biological research, vol. 245, 1987, pp. 411-3.

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Hai CM, Phair RD. "Kinetic identification of an intracellular calcium compartment sensitive to phosphate and dinitrophenol in intact isolated rabbit aorta." Circulation research, vol. 59, no. 1, 1986, pp. 85-92.

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Phair RD, Hai CM. "Resolution of intracellular calcium metabolism in intact segments of rabbit aorta." Circulation research, vol. 59, no. 1, 1986, pp. 74-84.

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Korecky B, Hai CM, Rakusan K. "Functional capillary density in normal and transplanted rat hearts." Canadian journal of physiology and pharmacology, vol. 60, no. 1, 1982, pp. 23-32.

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Research

Research Overview

Research Statement

Vascular and airway smooth muscle cell physiology, cell biology, and systems biology in relation to atherosclerosis, vasoconstriction, and asthma - are the foci of our research. We presently pursue the following research projects.

Nicotine-Induced Vascular Smooth Muscle Invasion.
Cigarette smoking is a significant risk factor for atherosclerosis, which involves the invasion of vascular smooth muscle cells (VSMCs) from the media to intima. A hallmark of many invasive cells is actin cytoskeletal remodeling in the form of podosomes, accompanied by extracellular matrix (ECM) degradation. A7r5 VSMCs form podosomes in response to PKC activation. We found that cigarette smoke extract, nicotine, and the cholinergic agonist, carbachol, were similarly effective in inducing the formation of podosome rosettes in A7r5 VSMCs. α-Bungarotoxin and atropine experiments confirmed the involvement of nicotinic acetylcholine receptors (nAChRs). Western blotting and immunofluorescence experiments revealed the aggregation of nAChRs at podosome rosettes. Cycloheximide experiments and media exchange experiments suggested that autocrine factor(s) and intracellular phenotypic modulation are putative mechanisms. In situ zymography experiments indicated that, in response to PKC activation, nicotine-treated cells degraded ECM near podosome rosettes, and possibly endocytose ECM fragments to intracellular compartments. Invasion assay of human aortic smooth muscle cells indicated that nicotine and PKC activation individually and synergistically enhanced cell invasion through ECM. We hypothesize that nicotine enhances the ability of VSMCs to degrade and invade ECM. nAChR activation, actin cytoskeletal remodeling and phenotypic modulation are possible mechanisms.

Systems Biology of Hemoglobin-Based Oxygen Carrier (HBOC)-Induced Vasoconstriction.
HBOCs are designed to carry oxygen to organ systems via the circulation. Unfortunately, HBOCs also scavenge nitric oxide (NO) - an important relaxing factor released by endothelial cells, and thereby reduces the availability of NO to vascular smooth muscle cells, disrupts NO-mediated cascade of signaling pathways in vascular smooth muscle cells, and causes vasoconstriction. Furthermore, in the presence of oxygen, HBOCs can undergo autoxidation with the generation of reactive oxygen species (ROS), which can lead to endothelial barrier dysfunction. HBOCs can then permeate through the leaky endothelial cell-cell junctions to the interstitial space near vascular smooth muscle cells, thereby further reducing the bioavailability of NO to vascular smooth muscle cells and causes vasoconstriction. The use of a single drug for attenuating HBOC-induced vasoconstriction has been tried with limited success. Since HBOC causes disruptions at multiple levels of organization in the vascular system, a systems approach is helpful to explore avenues to counteract the effects of HBOC at multiple levels by targeting multiple sites in the system. A multi-target approach is especially appropriate for HBOC-induced vasoconstriction, because HBOC disrupts the cascade of amplification by NO-cGMP signaling and protein phosphorylation, ultimately resulting in vasoconstriction. Identifying targets and doses for developing a multi-target combination HBOC regimen for oxygen therapeutics requires a detailed understanding of the systems biology and phenotypic heterogeneity of the vascular system at multiple layers of organization, which can be accomplished by successive iterations between experimental studies and mathematical modeling at multiple levels of vascular systems and organ systems.

Mechanosensitive Modulation of Cytoskeletal Remodeling in Airway Smooth Muscle.
Airway smooth muscle (ASM) hyperresponsiveness is an important problem in asthma. Recent studies indicated that bronchodilators are relatively ineffective in dilating closed airways in asthmatics, suggesting that mechanisms other than actomyosin crossbridge-based contraction may mediate airway closing in asthmatics. We have postulated that agonist-stimulated ASM functions as a hybrid biomaterial, capable of switching between functioning as a cytoskeleton-based viscoelastic body at short length and as a crossbridge-based contractile cell at long length. Accordingly, we hypothesize that phosphatidylinositol 4,5-bisphosphate (PIP2) functions as a length-dependent switch in mechanosensitive modulation of cytoskeletal recruitment and crossbridge cycling in agonist-stimulated ASM. PIP2 breakdown catalyzed by PLC is a major signal transduction mechanism for generating inositol trisphosphate and diacylglycerol for activating crossbridge cycling. In contrast, the PIP2 molecule itself also functions as an important signaling molecule, because PIP2 can recruit cytoplasmic proteins having phosphoinositide recognition domains to the cell membrane. Agonist-stimulated PIP2 breakdown is length-dependent in ASM; therefore, PIP2 content should be up-regulated at short muscle length and down-regulated at long muscle length. This hypothesis predicts that PIP2 content-dependent cytoskeletal recruitment and PIP2 breakdown-dependent crossbridge cycling should change in opposite directions as a function of muscle length. This prediction challenges the current paradigm that cytoskeletal recruitment and crossbridge cycling change in the same direction during contraction-relaxation cycles in ASM.

Funded Research

2008-2009 Principal Investigator, NIH R56 Research Grant Award (HL52714)

2007-2008 Principal Investigator, Naval Medical Research Center (N00189-07-C-Z086)

1996-2005 Principal Investigator, NIH R01 Research Grant Award (HL52714)

1991-1994 Principal Investigator, American Heart Association, National Center, Grant-in-Aud Award (91008460)

1989-1992 Principal Investigator, National Science Foundation Research Grant Award (8902438)

Scholarly Work

Gu, Z., V. Fonseca, and C.-M. Hai. Nicotinic acetylcholine receptor mediates nicotine-induced actin cytoskeletal remodeling and extracellular matrix degradation by vascular smooth muscle cells. Vascular Pharmacology, 2012 (doi: 10.1016/j.vph.2012.08.003).

Hai, C.M. Systems biology of HBOC-induced vasoconstriction. Curr. Drug. Discovery Technol. 9: 204-211, 2012

Aron, A.W., E.E. Macksoud, R.V. Iozzo, C.-M. Hai, and B.E. Lechner. Uterine dysfunction in biglycan and decorin deficient mice leads to dystocia during parturition. PLoS ONE 7: e29627, 2012

Kim, H.R., K. Liu, T.J. Roberts, and C.-M. Hai. Length-dependent modulation of cytoskeletal remodeling and mechanical energetics in airway smooth muscle. Am. J. Respir. Cell Mol. Biol. 44: 888-897, 2011

Fonseca, V., J. Avizinis, P. Moon-Massat, D. Freilich, H.W. Kim, and C.M. Hai. Differential sensitivities of pulmonary and coronary arteries to hemoglobin-based oxygen carriers and nitrovasodilators: Study in a bovine ex vivo model of vascular strips. Vasc. Pharmacol. 52: 215-223, 2010

Kim, H.-W., C.-M. Hai, and G. Greenburg. Acellular hemoglobin-based oxygen carrier induced vasoconstriction and hypertension: a brief review of potential pharmacologic remedies. Artificial Blood 17: 147-159, 2009

Hai, C.-M. Mechanistic systems biology of inflammatory expression in airway smooth muscle as tool for asthma drug development. Curr. Drug. Discovery Technol., 2008 (Accepted for Publication)

Hai, C.-M. Caldesmon as a therapeutic target for proliferative vascular diseases. Mini-Reviews in Medicinal Chemistry 8: 1209-1213, 2008

Hai, C.-M. Airway smooth muscle cell as therapeutic target of inflammation. Curr. Med. Chem. 14: 67-76, 2007

Gu, Z., J. Kordowska, G.L. Williams, C.-L.A. Wang, and C.-M. Hai. Erk1/2 MAPK and caldesmon differentially regulate podosome dynamics in A7r5 vascular smooth muscle cells. Exp. Cell Res. 313: 849-866, 2007

Kanefsky, J., M. Lenburg, and C.-M. Hai. Cholinergic receptor and cyclic stretch-mediated inflammatory gene expression in intact ASM. Am. J. Respir. Cell Mol. Biol. 34: 417-425, 2006

Hai, C.-M. and Z. Gu. Caldesmon phosphorylation in actin cytoskeletal remodeling. Eur. J. Cell Biol. 85: 305-309, 2006.

Kim, H.R. and C.-M. Hai. Mechanisms of mechanical strain memory in airway smooth muscle. Can. J. Physiol. Pharmacol. 83: 811-815, 2005

Hai, C.-M. and H.R. Kim. An expanded latch-bridge model of protein kinase C-mediated smooth muscle contraction. J. Appl. Physiol. 98:1356-1365, 2005

Lu, Q., E.O. Harrington, C.-M. Hai, J. Newton, M. Garber, T. Hirase, and S. Rounds. Isoprenylcysteine carboxyl methyltransferase modulates endothelial monolayer permeability. Involvement of RhoA carboxyl methylation. Circ. Res., 94: 306-315, 2004.

Kim, H.R., M. Hoque, and C.-M. Hai. Cholinergic receptor-mediated differential cytoskeletal recruitment of actin- and integrin-binding proteins in intact airway smooth muscle. Am. J. Physiol.: Cell Physiol. 287:.C1375-C1383, 2004

Wahl, M. and C.-M. Hai. Sinusoidal length oscillation and receptor-mediated mRNA expression of myosin isoforms and alpha-SM actin in airway smooth muscle. Am. J. Physiol. Cell Physiol. 287: C1697-C1708, 2004

Bai, T.R. et al. On the terminology for describing the length-force relationship and its changes in airway smooth muscle. J. Appl. Physiol. 97: 2029-2034, 2004.

Hai, C.-M., G. Sadowska, L. Francois, and B.S. Stonestreet. Maternal Dexamethasone Treatment Modulates Myosin Isoform Expression and Contractile Dynamics in Fetal Carotid Arteries. Am. J. Physiol. Heart Circ. Physiol. 283: H1743-H1749, 2002.

Hai, C.-M., P. Hahne, E.O Harrington, and M. Gimona. Conventional PKC mediates phorbol dibutyrate-induced cytoskeletal remodeling in A7r5 smooth muscle cells. Experimental Cell Research, 280:64-74, 2002.

Silberstein, J. and C.-M. Hai. Dynamics of length-force relations in airway smooth muscle. Respiratory Physiology & Neurobiology 132: 205-221, 2002.

Chan, W.L., J. Silberstein, and C.-M. Hai. Mechanical strain memory in airway smooth muscle. Am. J. Physiol. Cell Physiol. 278: C895-C904, 2000.

An, S.S. and C.-M. Hai. Mechanical signals and mechanosensitive modulation of intracellular [Ca2+] in smooth muscle. Am. J. Physiol. Cell Physiol. 279: C1375-C1384, 2000.

Hai, C.-M. Mechanosensitive modulation of receptor-mediated crossbridge activation and cytoskeletal organization in airway smooth muscle. Arch. Pharmacal Res. 23: 535-547, 2000.

An, S.S. and C.-M. Hai. Mechanical Strain Modulates Maximal Phosphatidylinositol Turnover in Airway Smooth Muscle. Am. J. Physiol 277 (Lung Cell. Mol. Physiol. 21): L968-L974, 1999.

Wong, C.T. and C.-M. Hai. Mucosal modulation of agonist-induced myosin phosphorylation and contraction in airway smooth muscle. Respiration Physiology 115: 103-111, 1999.

Youn, T., S.A. Kim, and C.-M. Hai. Length-dependent modulation of smooth muscle activation: effects of agonist, cytochalasin, and temperature. Am. J. Physiol. 274 (Cell Physiol. 43): C1601-1607, 1998.

Tseng, S., R. Kim, T. Kim, K.G. Morgan, and C.-M. Hai. F-actin disruption attenuates agonist-induced [Ca2+], myosin phosphorylation, and force in smooth muscle. Am. J. Physiol. 272 (Cell Physiol. 41): C1960-C1967, 1997.

Szeto, B. and C.-M. Hai. Length-dependent modulation of myosin phosphorylation and contractile force in coronary arterial smooth muscle. Arch. Biochem. Biophys. 329: 241-248, 1996.

Yoo, J., R. Ellis, K.G. Morgan, and C.-M. Hai. Mechanosensitive modulation of myosin phosphorylation and phosphatidylinositol turnover in smooth muscle. Am. J. Physiol. 267 (Cell Physiol. 36): C1657-C1665, 1994.

Background

Education and Training

Year	Degree	Institution
1984	PhD	The Johns Hopkins University
1980	MSc	University of Ottawa
1978	BSc	University of Toronto

Honors and Awards

2017 Brown University President’s Award for Excellence in Faculty Governance

2006 Dean's Teaching Excellence Award, Brown Medical School

2004 Dean's Teaching Excellence Award, Brown Medical School

2003 Exemplary Online Course Using WebCT Recognition for Biomed 117, Brown University

1983 Certificate of Merit for Young Investigators, Johns Hopkins University

Affiliations Visualize it

Collaborators

Name	Title
Lechner, Beatrice	Associate Professor of Pediatrics
Roberts, Thomas	Senior Associate Dean for the Program in Biology, Professor of Ecology, Evolution, and Organismal Biology

Affiliations

American Society for Cell Biologists
Invadosome Consortium

Researchers@Brown

Researchers@Brown

Chi-Ming Hai

Professor Emeritus of Molecular Pharmacology, Physiology and Biotechnology

Overview

Brown Affiliations

Research Areas

Publications Visualize it

Research

Research Overview

Research Statement

Funded Research

Scholarly Work

Background

Education and Training

Honors and Awards

Affiliations Visualize it

Collaborators

Affiliations

Teaching

Teaching Overview

Teaching