Role of CD38/cADPR signaling in obstructive pulmonary diseases

Alonso GP Guedes; Mythili Dileepan; Joseph A. Jude; Deepak A. Deshpande; Timothy F. Walseth; Mathur S. Kannan

doi:10.1016/j.coph.2020.04.007

Role of CD38/cADPR signaling in obstructive pulmonary diseases

Alonso GP Guedes, Mythili Dileepan, Joseph A. Jude, Deepak A. Deshpande, Timothy F. Walseth, Mathur S. Kannan

Research output: Contribution to journal › Review article › peer-review

11 Scopus citations

Abstract

The worldwide socioeconomical burden associated with chronic respiratory diseases is substantial. Enzymes involved in the metabolism of nicotinamide adenine dinucleotide (NAD) are increasingly being implicated in chronic airway diseases. One such enzyme, CD38, utilizes NAD to produce several metabolites, including cyclic ADP ribose (cADPR), which is involved in calcium signaling in airway smooth muscle (ASM). Upregulation of CD38 in ASM caused by exposure to cytokines or allergens leads to enhanced calcium mobilization by agonists and the development of airway hyperresponsiveness (AHR) to contractile agonists. Glucocorticoids and microRNAs can suppress CD38 expression in ASM, whereas cADPR antagonists such as 8Br-cADPR can directly antagonize intracellular calcium mobilization. Bronchodilators act via CD38-independent mechanisms. CD38-dependent mechanisms could be developed for chronic airway diseases therapy.

Original language	English (US)
Pages (from-to)	29-33
Number of pages	5
Journal	Current Opinion in Pharmacology
Volume	51
DOIs	https://doi.org/10.1016/j.coph.2020.04.007
State	Published - Apr 2020

Bibliographical note

Funding Information:
Mathur S. Kannan and Deepak A. Deshpande received support through grants from the National Institutes of Health .

Publisher Copyright:
© 2020 Elsevier Ltd

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title = "Role of CD38/cADPR signaling in obstructive pulmonary diseases",

abstract = "The worldwide socioeconomical burden associated with chronic respiratory diseases is substantial. Enzymes involved in the metabolism of nicotinamide adenine dinucleotide (NAD) are increasingly being implicated in chronic airway diseases. One such enzyme, CD38, utilizes NAD to produce several metabolites, including cyclic ADP ribose (cADPR), which is involved in calcium signaling in airway smooth muscle (ASM). Upregulation of CD38 in ASM caused by exposure to cytokines or allergens leads to enhanced calcium mobilization by agonists and the development of airway hyperresponsiveness (AHR) to contractile agonists. Glucocorticoids and microRNAs can suppress CD38 expression in ASM, whereas cADPR antagonists such as 8Br-cADPR can directly antagonize intracellular calcium mobilization. Bronchodilators act via CD38-independent mechanisms. CD38-dependent mechanisms could be developed for chronic airway diseases therapy.",

author = "Guedes, {Alonso GP} and Mythili Dileepan and Jude, {Joseph A.} and Deshpande, {Deepak A.} and Walseth, {Timothy F.} and Kannan, {Mathur S.}",

note = "Funding Information: Mathur S. Kannan and Deepak A. Deshpande received support through grants from the National Institutes of Health . Publisher Copyright: {\textcopyright} 2020 Elsevier Ltd",

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T1 - Role of CD38/cADPR signaling in obstructive pulmonary diseases

AU - Guedes, Alonso GP

AU - Dileepan, Mythili

AU - Jude, Joseph A.

AU - Deshpande, Deepak A.

AU - Walseth, Timothy F.

AU - Kannan, Mathur S.

PY - 2020/4

Y1 - 2020/4

N2 - The worldwide socioeconomical burden associated with chronic respiratory diseases is substantial. Enzymes involved in the metabolism of nicotinamide adenine dinucleotide (NAD) are increasingly being implicated in chronic airway diseases. One such enzyme, CD38, utilizes NAD to produce several metabolites, including cyclic ADP ribose (cADPR), which is involved in calcium signaling in airway smooth muscle (ASM). Upregulation of CD38 in ASM caused by exposure to cytokines or allergens leads to enhanced calcium mobilization by agonists and the development of airway hyperresponsiveness (AHR) to contractile agonists. Glucocorticoids and microRNAs can suppress CD38 expression in ASM, whereas cADPR antagonists such as 8Br-cADPR can directly antagonize intracellular calcium mobilization. Bronchodilators act via CD38-independent mechanisms. CD38-dependent mechanisms could be developed for chronic airway diseases therapy.

AB - The worldwide socioeconomical burden associated with chronic respiratory diseases is substantial. Enzymes involved in the metabolism of nicotinamide adenine dinucleotide (NAD) are increasingly being implicated in chronic airway diseases. One such enzyme, CD38, utilizes NAD to produce several metabolites, including cyclic ADP ribose (cADPR), which is involved in calcium signaling in airway smooth muscle (ASM). Upregulation of CD38 in ASM caused by exposure to cytokines or allergens leads to enhanced calcium mobilization by agonists and the development of airway hyperresponsiveness (AHR) to contractile agonists. Glucocorticoids and microRNAs can suppress CD38 expression in ASM, whereas cADPR antagonists such as 8Br-cADPR can directly antagonize intracellular calcium mobilization. Bronchodilators act via CD38-independent mechanisms. CD38-dependent mechanisms could be developed for chronic airway diseases therapy.

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Role of CD38/cADPR signaling in obstructive pulmonary diseases

Abstract

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