Acta Scientific Medical Sciences (ASMS)(ISSN: 2582-0931)

Research Article Volume 6 Issue 4

Potential Nucleotides of CD38 are Causing the Aggregation of Platelets

Mazhar Mushtaq*

Associate Professor, Basic Medical Sciences, Sulaiman Al Rajhi University, Saudi Arabia

*Corresponding Author: Mazhar Mushtaq, Associate Professor, Basic Medical Sciences, Sulaiman Al Rajhi University, Saudi Arabia.

Received: February 17, 2022; Published: March 15, 2022

Abstract

Objective: To elucidate the platelets aggregating effects of CD38 produced nucleotides.

Introduction: The production of cADPR and NAADP has been demonstrated in various cells in different tissues. Their primary physiological response is to elicit an increase in intracellular calcium. Platelets, like other cells, are also calcium dependent on producing their physiological response, normal aggregation.

Materials and Methods: The platelets aggregating effect was studied in thermomax microplate reader. Calcium measurements were carried out using Fura 2-AM loaded platelets subjected to PTI in a magnetically stirred cuvette at 37 °C with proper excitation wavelengths. cADPR and NAADP assay were performed using a fluorescence reader. Thrombin and ADP were used as physiological agonist along with cADPR and NAADP. Values of the result were expressed as mean and were considered statistically significant if p < 0.05.

Result: By using Thrombin and ADP, we were able to delineate the pathway of cADPR and NAADP and their response to releasing calcium from the intracellular organelles. The use of specific inhibitors in the paths of these nucleotides enabled us to deduce that cADPR is upstream to that of NAADP.

Keywords: CD38; cADPR; NAADP; Platelets; Calcium Signal

References

  1. George JN. “Platelets”. Lancet 355 (2000): 1531-1539.
  2. Mazhar Mushtaq., et al. “Critical Role for CD38-mediated Ca2+ Signaling in thrombin-induced Procoagulant Activity of Mouse Platelets and Hemostasis”. The Journal of Biological Chemistry 286 (2011): 12952-12958.
  3. Trevor j Shuttleworth. “Intracellular Ca2+ signalling in secretory cells”. The Journal of Experimental Biology 200 (1997): 303-314.
  4. So-Young Rah., et al. “Generation of cyclic ADP-ribose and nicotinic acid adenine dinucleotide phosphate by CD38 for Ca2+ signaling in interleukin-8-treated lymphokine-activated killer cells”. The Journal of Biological Chemistry 285 (2010): 21877-21887.
  5. Rukhsana Gul., et al. “Nicotinic Acid Adenine Dinucleotide Phosphate (NAADP) and Cyclic ADP-Ribose (cADPR) Mediate Ca2+ Signaling in Cardiac Hypertrophy Induced by β-Adrenergic Stimulation”. PLoS One 11 (2016): e0149125.
  6. Asif Iqbal Shawl 1., et al. “Insulin receptor signaling for the proliferation of pancreatic β-cells: involvement of Ca2+ second messengers, IP3, NAADP and cADPR”. Islets 3 (2009): 216-223.
  7. Byung JK., et al. “Generation of Nicotinic Acid Adenine Dinucleotide Phosphate and Cyclic ADP-Ribose by Glucagon-Like Peptide-1 Evokes Ca2+ Signal That Is Essential for Insulin Secretion in Mouse Pancreatic Islets”. Diabetes 57 (2008): 868-878.
  8. Lee HC. “Physiological functions of cADPR and NAADP as calcium messengers”. Annual Review of Pharmacology and Toxicology 41 (2001): 317-345.
  9. Fritz N., et al. “Ryanodine receptor subtype 2 encodes Ca2+ oscillations activated by acetylcholine via the M2 muscarinic receptor/cADP-ribose signalling pathway in duodenum myocytes”. Journal of Cell Science 118 (2005): 2261-2270.
  10. Dabertrand, F., et al. “Role of RYR3 splice variants in calcium signaling in mouse nonpregnant and pregnant myometrium”. American Journal of Physiology-Cell Physiology 293 (2007): 848-854.
  11. Park D-R., et al. “CD38-cADPR-SERCA signaling axis determines skeletal muscle contractile force in response to β-adrenergic stimulation”. Cellular Physiology and Biochemistry 46 (2018): 2017-2030.
  12. Guse AH., et al. “Ca2+ entry induced by cyclic ADP-ribose in intact T-lymphocytes”. Journal of Biological Chemistry 272 (1997): 8546-8550.
  13. Moccia F., et al. “NAADP activates a Ca2+ current that is dependent on F-actin cytoskeleton”. The FASEB Journal 13 (2003): 1907-1909.
  14. Lee VS., et al. “Quantitative optical determination of the viability of platelet concentrates”. Journal of Biomedical Engineering 14 (1992): 27-32.
  15. Bednar B., et al. “Platelet aggregation monitored in a 96 well microplate reader is useful for evaluation of platelet agonists and Antagonists”. Thrombosis Research 77 (1995): 453-463.
  16. Ribeiro José MC., et al. “Platelet activating factor hydrolyzing phospholipase C in the salivary glands and saliva of the mosquito Culex quinquefasciatus”. The Journal of Experimental Biology 204 (2001): 3887-3894.
  17. Rah SY., et al. “Activation of CD38 by interleukin-8 Signaling regulates intracellular Ca2+ level and motility of lymphokines activated Killer cells”. Journal of Biological Chemistry 280 (2005): 2888-2895.
  18. R A Billington., et al. “A transport mechanism for NAADP in a rat basophilic cell line”. The FASEB Journal 20 (2006): 521-523.
  19. Robert Flaumenhaft. “Molecular Basis of Platelet Granule Secretion”. Arteriosclerosis, Thrombosis, and Vascular Biology 23 (2003): 1152-1160.
  20. Smith J B and Willis A L. Nature (London) New Biology 231 (1971): 235-237.
  21. Chen-Yi Su. “Differential Effects of Ganodermic Acid S on the Thromboxane A2-Signaling Pathways in Human”. Platelets Biochemistry and Pharmacology 58 (1999): 587-595.
  22. Xin Tang. “Role of phospholipase C and diacylglyceride lipase pathway in arachidonic acid release and acetylcholine-induced vascular relaxation in rabbit aorta”. American Journal of Physiology-Heart and Circulatory Physiology 290 (2006): H37-H45.
  23. Mihaly K., et al. “Mechanism of Blebbistatin Inhibition of Myosin II”. The Journal of Biological Chemistry 279 (2004): 35557-35563.
  24. Bhagavathi R., et al. “Kinetic Mechanism of Blebbistatin Inhibition of Nonmuscle Myosin IIB”. Biochemistry 43 (2004): 14832-14839.
  25. Rah SY. “Association of CD38 with non-muscle myosin heavy chain IIA and Lck is essential for the internalization and activation of CD38”. Journal of Biological Chemistry 282 (2006): 5653-5660.
  26. Richard AB., et al. “Production and characterization of reduced NAADP (nicotinic acid-adenine dinucleotide phosphate)”. Biochemistry Journal 378 (2004): 275-280.

Citation

Citation: Mazhar Mushtaq. “Potential Nucleotides of CD38 are Causing the Aggregation of Platelets”.Acta Scientific Medical Sciences 6.4 (2022): 100-106.

Copyright

Copyright: © 2022 Mazhar Mushtaq. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.




Metrics

Acceptance rate30%
Acceptance to publication20-30 days
Impact Factor1.403

Indexed In





Contact US