Molecular and Cellular Physiology
Ph.D. in Pharmacology, University of Cambridge, 1989;
Postdoctoral Positions, Dept. Pharmacology, Yale Univ. School of Medicine, and Dept. of Surgery, Harvard Medical School and Beth Isreal Hospital, 1990-1994;
Associate Professor, National Laboratory of Biotechnology, China Agricultural University, 1994-1998;
Professor, Beijing Normal University, 1998 - Present.
Editorial Boards: Prog Physiol Sci, Biophys Rep (Associate Editor), Pancreapedia.
Undergraduate Course (A Nationally Acclaimed Course): Human and Animal Physiology.
1. Cytosolic Calcium Oscillations: Among the earliest responses after cellular stimulation is increase in cytosolic calcium concentration. Such calcium increases in individual cells are often in the form of oscillations - periodic increases in cytoslic calcium concentrtion. Oscillation confers two forms of modultion of the calcium signal: amplitude modultion (AM), and frequency modultion (FM), therefore multiple calcium signals could be encoded, to modulate specific cellular functions. Our laboratory investigates in secretory and other cell types the molecular mechanisms of calcium oscillations, such as a role for TLR9-ORAI1, NCX, and ER calcium channels in the pace-making process of calcium oscillations.
2. Molecular Basis of Exocytosis: Secretory cells are pivotal in the body. Secretory cells such as pancreatic acinar cells, pancreatic islet beta cells, anterior pituitary cells, mamary gland acinar cells, after stimulation by neurotransmitters or hormones all have their secretory granules in the cytosol to dock at, and fuse with, the plasma membrane, subsequently to release the granule content into the extracellular space. Our laboratory investigates how after stimulation, secretory cells have their secretory granules dock at, and fuse with plasma membrane, to complete the process of exocytosis and cell secretion, with an emphasis on SNARE and related proteins. Photodynamic modulations of the SNARE exocytotic and protein transport processes with genetically encoded protein photosensitisers are investigated.
3. Singlet Oxygen As A Signaling Molecule: Many chromophores (photon-absorbing groups) in nature could absorb photons of certain wavelength. When such molecules after absorption of photons transfer their photon energy to molecular oxygen, the excited delta singlet oxygen is produced. Since singlet oxygen has very high chemical energy (94 kJ/mole), and a very short lifetime in cellular environment (1 μs), it has very limited distance of effective reaction (< 10 nm). Therefore singlet oxygen generated during a Type II photodynamic action could subcellular specifically modulate cellular functions. Our laboratory investigates molecular targets of photodynamic action in living cells, and the resultant chemical modifications of biologically important signaling proteins such as G protein-coupled receptors and voltage-gated ionic channels. We also investigate the molecular basis of singlet oxygen action as an endogenous signaling molecule.
4. Modulation Of Synaptic Transmission By Toosendanin: To examine the cellular and molecular effects of toosendanin on synaptic transmission.
5. Contact Regulation Between Neighboring Cell Types: To investigate regulation by neutrophil respiratory burst, pancreatic stellate cell activation on pancreatic acinar calcium signalling. Recently it was found that the pancreatic stellate cells exert on the pancreatic acinar cell calcium signaling a braking mechanism.
Recruitments for MPhil / PhD students and postdoctoral fellows:
071009 Cell Biology Program - Signaling In Secretory Cells
♦ Research Articles
1. Li Y, Cui ZJ (2020) NanoLuc bioluminescence-driven photodynamic activation of cholecystokinin 1 receptor with genetically encoded protein photosensitiser miniSOG. Intl J Mol Sci 21: 3763. https://www.mdpi.com/1422-0067/21/11/3763
2. Tang WZ, Cui ZJ (2020) Permanent photodynamic activation of the cholecystokinin 2 receptor. Biomolecules 10: 236. https://www.mdpi.com/2218-273X/10/2/236
3. Liu JS & Cui ZJ (2019) Pancreatic stellate cells serve as a brake mechanism on pancreatic acinar cell calcium signaling modulated by methionine sulfoxide reductase expression. Cells 8: 109. https://www.mdpi.com/2073-4409/8/2/109
4. Guo HY & Cui ZJ (2019) Extracellular histones activate TLR9 to induce calcium oscillations in rat pancreatic acinar tumor cell AR4-2J. Cells 8: 3. https://www.mdpi.com/2073-4409/8/1/3
5. Jiang WY, Li Y, Li ZY & Cui ZJ (2018) Permanent photodynamic cholecystokinin 1 receptor activation-dimer-to-monomer conversion. Cell Mol Neurobiol 38: 1283-1292.
6. Jiang HN, Li Y, Jiang WY & Cui ZJ (2018) Cholecystokinin 1 receptor-a unique G protein-coupled receptor activated by singlet oxygen (GPCR-ABSO). Front Physiol 9: 497. https://www.frontiersin.org/articles/10.3389/fphys.2018.00497/full
7. Liang HY, Song ZM & Cui ZJ (2013) Lasting inhibition of receptor-mediated calcium oscillations in pancreaticacini by neutrophil respiratory burst - a novel mechanism for secretory blockade in acute pancreatitis? BiochemBiophys Res Commun 437: 361-367.
8. Jia YH & Cui ZJ (2011) Tri-phasic modulation of ACh- and NE-maintained calcium plateau by high potassium in isolated mouse submandibular granular convoluted tubular cells. Arch Oral Biol 56: 1347-1355.
9. Fang XF & Cui ZJ (2011) The anti-botulism triterpenoid toosendanin elicits calcium increase and exocytosis in rat sensory neurons. Cell Mol Neurobiol 31: 1151-1162.
10. Duan YJ, Liang HY, Jin WJ, Cui ZJ (2011) Substance P conjugated to CdTe quantum dot triggers cytosolic calcium oscillations and induces QD internalization in the pancreatic carcinoma cell line AR4-2J. Analyt Bioanalyt Chem 400: 2995-3003.
11. Chen BD, Guan DD, Cui ZJ, Wang X & Shen X (2010) Thioredoxin 1 downregulates MCP-1 secretion and expression in human endothelial cells by suppressing nuclear translocation of activator protein 1 and redox factor-1. Am J Physiol Cell Physiol 298: C1170-C1179.
12. Wang BJ, Liang HY & Cui ZJ (2009) Duck pancreatic acinar cell as a unique model for independent cholinergic stimulation-secretion coupling. Cell Mol Neurobiol 29: 747-756.
13. Zhou YD, Fang XF & Cui ZJ (2009) UVA induced calcium oscillations in rat mast cells. Cell Calcium 45: 18-28. (Zhou YD: https://profiles.psu.edu/profiles/display/73800983)
14. Hu F, Sun WW, Zhao XT, Cui ZJ & Yang WX (2008) TRPV1 mediates cell death in rat synovial fibroblasts through calcium entry-dependent ROS production and mitochondrial depolarization. Biochem Biophys Res Commun 369: 989-993.
15. Ma CY & Cui ZJ (2004) Selective use of a reserved mechanism for inducing calcium oscillations. Cell Signal 16: 1435-1440.
16. Xiao R & Cui ZJ (2004) Mutual dependence of VIP/PACAP and CCK receptor signaling for a physiological role in duck exocrine pancreatic secretion. Am J Physiol 286: R189-R198. (Xiao R: http://aging.ufl.edu/profile/rui-xiao-ph-d/)
17. Cui ZJ, Zhou YD, Satoh Y & Habara Y (2003) A physiological role for protoporphyrin IX photodynamic action in the rat Harderian gland? Act Physiol Scand 179: 149-154.
18. An YP, Xiao R, Cui H & Cui ZJ (2003) Selective activation by photodynamic action of cholecystokinin receptor in the freshly isolated rat pancreatic acini. Br J Pharmacol 139: 872-880.
1. Jiang HN, Li Y & Cui ZJ (2017) Photodynamic physiology-photonanomanipulations in cellular physiology with protein photosensitisers. Front Physiol 8: 191.
2. Cui ZJ, Han ZQ & Li ZY (2012) Modulating protein activity and cellular function by methionine residue oxidation. Amino Acids 43: 505-517.
3. Wang BJ & Cui ZJ (2007) How does cholecystokinin stimulate exocrine pancreatic secretion? From birds, rodents, to humans. Am J Physiol 292: R666-R678.
Institute of Cell Biology,
Beijing Normal University,
Beijing 100875, China
Tel: +86 10 5880 9162