Saliva, a complex fluid secreted by salivary glands, is of critical importance to the health of the oral cavity. Neurotransmitter mediated calcium mobilization in salivary glands regulates the formation and secretion of saliva and is of primary importance to the salivary cell. To investigate the mechanisms regulating cytosolic calcium during secretory events, we have utilized in vitro dispersed cell and cellular membrane vesicle preparations from rat parotid glands. These studies have been directed towards understanding at a molecular level, (i) the basic mechanisms of calcium transport involved in the establishment of cellular calcium homeostasis; and (ii) the modulation of thee processes during neurotransmitter induced calcium mobilization. It has been shown previously that alpha 1-adrenergic and muscarinic receptor stimulation lead to calcium efflux from parotid cells. It was also shown that basolateral membrane vesicles isolated from parotid gland possess an ATP-dependent calcium transporter, which is one of the major systems regulating cytosolic calcium. In the present reporting period we have characterized the calcium transporting activities associated with two major membrane systems in the parotid cell. In the basolateral membrane we have (i) studied the modulation of the ATP dependent calcium transport by secondary ion movements and by membrane sulfhydryl group modification, (ii) developed a reconstituted system of this transporter in artifical lipid vesicles, (iii) established the electrogenic nature of the sodium/calcium exchanger. In the endoplasmic reticulum, we have characterized the ATP + magnesium-dependent calcium pump and its ionic correlates. We have also studied beta-adrenoreceptor mediated calcium mobilization in rat parotid cells in order to identify the signalling events leading to modification of calcium transport.

Agency
National Institute of Health (NIH)
Institute
National Institute of Dental & Craniofacial Research (NIDCR)
Type
Intramural Research (Z01)
Project #
1Z01DE000438-02
Application #
3939988
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
2
Fiscal Year
1987
Total Cost
Indirect Cost
Name
Dental & Craniofacial Research
Department
Type
DUNS #
City
State
Country
United States
Zip Code
Liu, Xibao; Gong, Baijuan; de Souza, Lorena Brito et al. (2017) Radiation inhibits salivary gland function by promoting STIM1 cleavage by caspase-3 and loss of SOCE through a TRPM2-dependent pathway. Sci Signal 10:
Ambudkar, Indu S (2016) Calcium signalling in salivary gland physiology and dysfunction. J Physiol 594:2813-24
Ma, Xin; Cheng, Kwong-Tai; Wong, Ching-On et al. (2011) Heteromeric TRPV4-C1 channels contribute to store-operated Ca(2+) entry in vascular endothelial cells. Cell Calcium 50:502-9
Nandula, Seshagiri R; Amarnath, Shoba; Molinolo, Alfredo et al. (2007) Female mice are more susceptible to developing inflammatory disorders due to impaired transforming growth factor beta signaling in salivary glands. Arthritis Rheum 56:1798-805
Vag, Janos; Byrne, Elaine M; Hughes, Deirdre H et al. (2007) Morphological and functional differentiation of HSG cells: role of extracellular matrix and trpc 1. J Cell Physiol 212:416-23
Ambudkar, Indu S; Ong, Hwei Ling (2007) Organization and function of TRPC channelosomes. Pflugers Arch 455:187-200
Ambudkar, I S (2007) Trafficking of TRP channels: determinants of channel function. Handb Exp Pharmacol :541-57
Ong, Hwei L; Liu, Xibao; Sharma, Ajay et al. (2007) Intracellular Ca(2+) release via the ER translocon activates store-operated calcium entry. Pflugers Arch 453:797-808
Ambudkar, I S (2007) TRPC1: a core component of store-operated calcium channels. Biochem Soc Trans 35:96-100
Ambudkar, Indu S; Ong, Hwei Ling; Liu, Xibao et al. (2007) TRPC1: the link between functionally distinct store-operated calcium channels. Cell Calcium 42:213-23

Showing the most recent 10 out of 48 publications