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Article ; Online: Antagonizing cholecystokinin A receptor in the lung attenuates obesity-induced airway hyperresponsiveness.

Panganiban, Ronald Allan M / Yang, Zhiping / Sun, Maoyun / Park, Chan Young / Kasahara, David I / Schaible, Niccole / Krishnan, Ramaswamy / Kho, Alvin T / Israel, Elliot / Hershenson, Marc B / Weiss, Scott T / Himes, Blanca E / Fredberg, Jeffrey J / Tantisira, Kelan G / Shore, Stephanie A / Lu, Quan

Nature communications

2023 Volume 14, Issue 1, Page(s) 47

Abstract: Obesity increases asthma prevalence and severity. However, the underlying mechanisms are poorly understood, and consequently, therapeutic options for asthma patients with obesity remain limited. Here we report that cholecystokinin-a metabolic hormone ... ...

Abstract	Obesity increases asthma prevalence and severity. However, the underlying mechanisms are poorly understood, and consequently, therapeutic options for asthma patients with obesity remain limited. Here we report that cholecystokinin-a metabolic hormone best known for its role in signaling satiation and fat metabolism-is increased in the lungs of obese mice and that pharmacological blockade of cholecystokinin A receptor signaling reduces obesity-associated airway hyperresponsiveness. Activation of cholecystokinin A receptor by the hormone induces contraction of airway smooth muscle cells. In vivo, cholecystokinin level is elevated in the lungs of both genetically and diet-induced obese mice. Importantly, intranasal administration of cholecystokinin A receptor antagonists (proglumide and devazepide) suppresses the airway hyperresponsiveness in the obese mice. Together, our results reveal an unexpected role for cholecystokinin in the lung and support the repurposing of cholecystokinin A receptor antagonists as a potential therapy for asthma patients with obesity.
MeSH term(s)	Animals ; Mice ; Asthma/drug therapy ; Asthma/metabolism ; Cholecystokinin/metabolism ; Lung/metabolism ; Mice, Obese ; Obesity/complications ; Obesity/metabolism ; Receptor, Cholecystokinin A/genetics ; Receptor, Cholecystokinin A/metabolism ; Respiratory Hypersensitivity/drug therapy ; Respiratory Hypersensitivity/metabolism
Chemical Substances	Cholecystokinin (9011-97-6) ; Receptor, Cholecystokinin A
Language	English
Publishing date	2023-01-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-35739-8
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Radiation-induced accelerated senescence: a fate worse than death?

Day, Regina M / Snow, Andrew L / Panganiban, Ronald Allan M

Cell cycle (Georgetown, Tex.)

2014 Volume 13, Issue 13, Page(s) 2011–2012

MeSH term(s)	Cellular Senescence/drug effects ; Cellular Senescence/radiation effects ; Endothelial Cells/cytology ; Humans ; Receptor, IGF Type 1/antagonists & inhibitors
Chemical Substances	Receptor, IGF Type 1 (EC 2.7.10.1)
Language	English
Publishing date	2014-06-05
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
DOI	10.4161/cc.29457
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Article ; Online: Correction

Ronald Allan M. Panganiban / Regina M. Day

PLoS ONE, Vol 9, Iss

Inhibition of IGF-1R Prevents Ionizing Radiation-Induced Primary Endothelial Cell Senescence

2014 Volume 1

Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2014-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Correction

Ronald Allan M. Panganiban / Regina M. Day

PLoS ONE, Vol 9, Iss

Inhibition of IGF-1R Prevents Ionizing Radiation-Induced Primary Endothelial Cell Senescence.

2014 Volume 1

Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2014-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Captopril reduces lung inflammation and accelerated senescence in response to thoracic radiation in mice.

Mungunsukh, Ognoon / George, Jeffy / McCart, Elizabeth A / Snow, Andrew L / Mattapallil, Joseph J / Mog, Steven R / Panganiban, Ronald Allan M / Bolduc, David L / Rittase, W Bradley / Bouten, Roxane M / Day, Regina M

Journal of radiation research

2021 Volume 62, Issue 2, Page(s) 236–248

Abstract: The lung is sensitive to radiation and exhibits several phases of injury, with an initial phase of radiation-induced pneumonitis followed by delayed and irreversible fibrosis. The angiotensin-converting enzyme inhibitor captopril has been demonstrated to ...

Abstract	The lung is sensitive to radiation and exhibits several phases of injury, with an initial phase of radiation-induced pneumonitis followed by delayed and irreversible fibrosis. The angiotensin-converting enzyme inhibitor captopril has been demonstrated to mitigate radiation lung injury and to improve survival in animal models of thoracic irradiation, but the mechanism remains poorly understood. Here we investigated the effect of captopril on early inflammatory events in the lung in female CBA/J mice exposed to thoracic X-ray irradiation of 17-17.9 Gy (0.5-0.745 Gy min-1). For whole-body + thoracic irradiation, mice were exposed to 7.5 Gy (0.6 Gy min-1) total-body 60Co irradiation and 9.5 Gy thoracic irradiation. Captopril was administered orally (110 mg kg-1 day-1) in the drinking water, initiated 4 h through to150 days post-irradiation. Captopril treatment increased survival from thoracic irradiation to 75% at 150 days compared with 0% survival in vehicle-treated animals. Survival was characterized by a significant decrease in radiation-induced pneumonitis and fibrosis. Investigation of early inflammatory events showed that captopril significantly attenuated macrophage accumulation and decreased the synthesis of radiation-induced interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) pro-inflammatory cytokines in the lungs of irradiated mice. Suppression of IL-1β and TNF-α correlated with an increase of the anti-inflammatory cytokine IL-10 in the spleen with captopril treatment. We also found that captopril decreased markers for radiation-induced accelerated senescence in the lung tissue. Our data suggest that suppression of inflammation and senescence markers, combined with an increase of anti-inflammatory factors, are a part of the mechanism for captopril-induced survival in thoracic irradiated mice.
MeSH term(s)	Aging/pathology ; Animals ; Apoptosis/drug effects ; Apoptosis/radiation effects ; Biomarkers/metabolism ; Captopril/pharmacology ; Captopril/therapeutic use ; Cytokines/metabolism ; Female ; Inflammation Mediators/metabolism ; Lung/drug effects ; Lung/radiation effects ; Macrophages, Alveolar/drug effects ; Macrophages, Alveolar/pathology ; Macrophages, Alveolar/radiation effects ; Mice, Inbred CBA ; Pneumonia/drug therapy ; Pulmonary Fibrosis/pathology ; Spleen/drug effects ; Spleen/radiation effects ; Survival Analysis ; Thorax/radiation effects ; Whole-Body Irradiation ; X-Rays ; Mice
Chemical Substances	Biomarkers ; Cytokines ; Inflammation Mediators ; Captopril (9G64RSX1XD)
Language	English
Publishing date	2021-02-22
Publishing country	England
Document type	Journal Article
ZDB-ID	603983-2
ISSN	1349-9157 ; 0449-3060
ISSN (online)	1349-9157
ISSN	0449-3060
DOI	10.1093/jrr/rraa142
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Article ; Online: Mechanisms of radiation toxicity in transformed and non-transformed cells.

Panganiban, Ronald-Allan M / Snow, Andrew L / Day, Regina M

International journal of molecular sciences

2013 Volume 14, Issue 8, Page(s) 15931–15958

Abstract: Radiation damage to biological systems is determined by the type of radiation, the total dosage of exposure, the dose rate, and the region of the body exposed. Three modes of cell death-necrosis, apoptosis, and autophagy-as well as accelerated senescence ...

Abstract	Radiation damage to biological systems is determined by the type of radiation, the total dosage of exposure, the dose rate, and the region of the body exposed. Three modes of cell death-necrosis, apoptosis, and autophagy-as well as accelerated senescence have been demonstrated to occur in vitro and in vivo in response to radiation in cancer cells as well as in normal cells. The basis for cellular selection for each mode depends on various factors including the specific cell type involved, the dose of radiation absorbed by the cell, and whether it is proliferating and/or transformed. Here we review the signaling mechanisms activated by radiation for the induction of toxicity in transformed and normal cells. Understanding the molecular mechanisms of radiation toxicity is critical for the development of radiation countermeasures as well as for the improvement of clinical radiation in cancer treatment.
MeSH term(s)	Apoptosis/radiation effects ; Autophagy/radiation effects ; Cell Line, Transformed ; Cellular Senescence/radiation effects ; Humans ; Necrosis ; Neoplasms ; Radiation Tolerance ; Radiation, Ionizing ; Signal Transduction/radiation effects
Language	English
Publishing date	2013-07-31
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms140815931
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Article ; Online: X-irradiation induces ER stress, apoptosis, and senescence in pulmonary artery endothelial cells.

Panganiban, Ronald Allan M / Mungunsukh, Ognoon / Day, Regina M

International journal of radiation biology

2013 Volume 89, Issue 8, Page(s) 656–667

Abstract: Purpose: The use of clinical radiation for cancer treatment is limited by damage to underlying normal tissue including to the vascular endothelium. We investigated the mechanisms of X-ray-induced cell damage to endothelial cells.: Methods: We ... ...

Abstract	Purpose: The use of clinical radiation for cancer treatment is limited by damage to underlying normal tissue including to the vascular endothelium. We investigated the mechanisms of X-ray-induced cell damage to endothelial cells. Methods: We evaluated necrosis, apoptosis, cellular senescence, and the contribution of endoplasmic reticulum (ER) stress in pulmonary artery endothelial cells (PAEC) irradiated with X-rays (2-50 Gray [Gy]). Results: Clonogenic assays showed that 10 Gy induced ∼99.9% loss of cell viability. No necrosis was detected using lactate dehydrogenase assays, but a low population underwent extrinsic and intrinsic apoptosis, as indicated by the activation of caspases 3, 8, and 9 as well as by neutral comet assay. A majority of PAEC underwent accelerated senescence, as indicated by morphological changes, increased 21 kD cyclin-dependent kinase inhibitor (p21/waf1), decreased sirtuin 1 (SIRT1), and elevated senescence-associated β-galactosidase (SA-β-gal). ER stress was detected by assays for glucose-regulated protein 78 (GRP78), CCAAT/enhancer-binding protein homologous protein (CHOP), and growth arrest and DNA damage-inducible protein 34 (GADD34) mRNA, and transient phosphorylation of eukaryotic translation initiation factor 2 alpha (eIF2α). The ER stress inhibitor salubrinal blocked ∼50% of apoptosis with no effect on senescence. Conclusions: X-rays primarily induced cellular senescence with limited levels of apoptosis in endothelial cells. ER stress contributed to apoptosis but not to senescence.
MeSH term(s)	Animals ; Apoptosis/radiation effects ; Cattle ; Cell Survival/radiation effects ; Cellular Senescence/radiation effects ; Dose-Response Relationship, Radiation ; Endoplasmic Reticulum Stress/radiation effects ; Endothelial Cells/cytology ; Endothelial Cells/radiation effects ; Pulmonary Artery/cytology ; Time Factors ; X-Rays/adverse effects
Language	English
Publishing date	2013-08
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	3065-x
ISSN	1362-3095 ; 0020-7616 ; 0955-3002
ISSN (online)	1362-3095
ISSN	0020-7616 ; 0955-3002
DOI	10.3109/09553002.2012.711502
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Article ; Online: Inhibition of IGF-1R prevents ionizing radiation-induced primary endothelial cell senescence.

Panganiban, Ronald Allan M / Day, Regina M

PloS one

2013 Volume 8, Issue 10, Page(s) e78589

Abstract: Accelerated senescence is a primary response to cellular stresses including DNA damaging agents (e.g., ionizing radiation) and is widely believed to be caused by continuous proliferative signaling in the presence of cell cycle arrest. Studies of signal ... ...

Abstract	Accelerated senescence is a primary response to cellular stresses including DNA damaging agents (e.g., ionizing radiation) and is widely believed to be caused by continuous proliferative signaling in the presence of cell cycle arrest. Studies of signal transduction pathways leading to accelerated senescence have revealed that inhibition of mammalian target of rapamycin (mTOR) by rapamycin rescues cells from senescence. However, the molecular mechanisms upstream of mTOR following ionizing radiation (IR) are not well defined. We investigated signal transduction leading to IR-induced accelerated senescence in human pulmonary artery endothelial cells (HPAEC). Exposure of HPAEC to X-rays (10 Gy, 2.4 Gy/min) upregulated senescence markers including p53, p21/waf1, and senescence-associated beta galactosidase (SA-β-gal). Ly294002 (a phosphatidylinositol-3-kinase [PI3K] inhibitor) or rapamycin (an mTOR inhibitor) blocked the induction of cellular senescence markers suggesting roles for PI3K and mTOR. Pathway-directed microarrays revealed increased transcription of insulin-like growth factor I (IGF-1), a modulator of cell growth and proliferation upstream of mTOR. qRT-PCR confirmed that both IGF-1 and IGF-2 mRNA were increased in response to X-rays, and ELISA showed increased secretion of IGF-1 protein into the medium of irradiated HPAEC. Consistent with upregulation of these ligands, we found that X-ray exposure led to hyperphosphorylation of IGF-1R, the receptor for IGF-1 and -2. Treatment with AG1024, an IGF-1R inhibitor, suppressed IR-induced upregulation of p53, p21/waf1, and SA-β-gal. Together these findings suggest that IGF-1R is a key regulator of IR-induced accelerated senescence in a pathway that requires intact mTOR activity upstream of both p53 and p21/waf1.
MeSH term(s)	Cellular Senescence/drug effects ; Cellular Senescence/radiation effects ; Endothelial Cells/cytology ; Endothelial Cells/drug effects ; Endothelial Cells/radiation effects ; Humans ; Lung/cytology ; Phenotype ; Phosphoinositide-3 Kinase Inhibitors ; Phosphorylation/drug effects ; Phosphorylation/radiation effects ; Reactive Oxygen Species/metabolism ; Receptor, IGF Type 1/antagonists & inhibitors ; Signal Transduction/drug effects ; Signal Transduction/radiation effects ; TOR Serine-Threonine Kinases/antagonists & inhibitors ; Time Factors ; Tyrphostins/pharmacology ; X-Rays/adverse effects
Chemical Substances	Phosphoinositide-3 Kinase Inhibitors ; Reactive Oxygen Species ; Tyrphostins ; tyrphostin AG 1024 ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Receptor, IGF Type 1 (EC 2.7.10.1)
Language	English
Publishing date	2013-10-24
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0078589
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Article ; Online: Inhibition of IGF-1R prevents ionizing radiation-induced primary endothelial cell senescence.

Ronald Allan M Panganiban / Regina M Day

PLoS ONE, Vol 8, Iss 10, p e

2013 Volume 78589

Abstract	Accelerated senescence is a primary response to cellular stresses including DNA damaging agents (e.g., ionizing radiation) and is widely believed to be caused by continuous proliferative signaling in the presence of cell cycle arrest. Studies of signal transduction pathways leading to accelerated senescence have revealed that inhibition of mammalian target of rapamycin (mTOR) by rapamycin rescues cells from senescence. However, the molecular mechanisms upstream of mTOR following ionizing radiation (IR) are not well defined. We investigated signal transduction leading to IR-induced accelerated senescence in human pulmonary artery endothelial cells (HPAEC). Exposure of HPAEC to X-rays (10 Gy, 2.4 Gy/min) upregulated senescence markers including p53, p21/waf1, and senescence-associated beta galactosidase (SA-β-gal). Ly294002 (a phosphatidylinositol-3-kinase [PI3K] inhibitor) or rapamycin (an mTOR inhibitor) blocked the induction of cellular senescence markers suggesting roles for PI3K and mTOR. Pathway-directed microarrays revealed increased transcription of insulin-like growth factor I (IGF-1), a modulator of cell growth and proliferation upstream of mTOR. qRT-PCR confirmed that both IGF-1 and IGF-2 mRNA were increased in response to X-rays, and ELISA showed increased secretion of IGF-1 protein into the medium of irradiated HPAEC. Consistent with upregulation of these ligands, we found that X-ray exposure led to hyperphosphorylation of IGF-1R, the receptor for IGF-1 and -2. Treatment with AG1024, an IGF-1R inhibitor, suppressed IR-induced upregulation of p53, p21/waf1, and SA-β-gal. Together these findings suggest that IGF-1R is a key regulator of IR-induced accelerated senescence in a pathway that requires intact mTOR activity upstream of both p53 and p21/waf1.
Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2013-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
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Article ; Online: Hepatocyte growth factor in lung repair and pulmonary fibrosis.

Panganiban, Ronald Allan M / Day, Regina M

Acta pharmacologica Sinica

2010 Volume 32, Issue 1, Page(s) 12–20

Abstract: Pulmonary remodeling is characterized by the permanent and progressive loss of the normal alveolar architecture, especially the loss of alveolar epithelial and endothelial cells, persistent proliferation of activated fibroblasts, or myofibroblasts, and ... ...

Abstract	Pulmonary remodeling is characterized by the permanent and progressive loss of the normal alveolar architecture, especially the loss of alveolar epithelial and endothelial cells, persistent proliferation of activated fibroblasts, or myofibroblasts, and alteration of extracellular matrix. Hepatocyte growth factor (HGF) is a pleiotropic factor, which induces cellular motility, survival, proliferation, and morphogenesis, depending upon the cell type. In the adult, HGF has been demonstrated to play a critical role in tissue repair, including in the lung. Administration of HGF protein or ectopic expression of HGF has been demonstrated in animal models of pulmonary fibrosis to induce normal tissue repair and to prevent fibrotic remodeling. HGF-induced inhibition of fibrotic remodeling may occur via multiple direct and indirect mechanisms including the induction of cell survival and proliferation of pulmonary epithelial and endothelial cells, and the reduction of myofibroblast accumulation.
MeSH term(s)	Animals ; Gene Expression ; Hepatocyte Growth Factor/genetics ; Hepatocyte Growth Factor/metabolism ; Humans ; Lung/cytology ; Lung/metabolism ; Lung/pathology ; Myofibroblasts/metabolism ; Pulmonary Fibrosis/metabolism ; Pulmonary Fibrosis/pathology ; Wound Healing
Chemical Substances	Hepatocyte Growth Factor (67256-21-7)
Language	English
Publishing date	2010-12-06
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1360774-1
ISSN	1745-7254 ; 0253-9756 ; 1671-4083
ISSN (online)	1745-7254
ISSN	0253-9756 ; 1671-4083
DOI	10.1038/aps.2010.90
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