Associate Professor of Medicine, Brigham and Women's Hospital
Pulmonology
Dr. Mark A. Perrella, MD
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Mark A. Perrella practices Pulmonology. He went to University of Nebraska College of Medicine. He received 1 awards: "Elected Member". Doctor Mark A. Perrella, MD has written publications. He has 47 publications published with PubMed. The lastest publication is: 'A Chronic Obstructive Pulmonary Disease Susceptibility Gene, FAM13A, Regulates Protein Stability of -catenin.' He accepts Medicare.
Publications
- Elk-3 is a KLF4-regulated gene that modulates the phagocytosis of bacteria by macrophages.
- Carbon monoxide confers protection in sepsis by enhancing beclin 1-dependent autophagy and phagocytosis.
- Gene expression analysis uncovers novel hedgehog interacting protein (HHIP) effects in human bronchial epithelial cells.
- Lipoxin a4 regulates natural killer cell and type 2 innate lymphoid cell activation in Asthma.
- Mesenchymal stromal cells improve survival during sepsis in the absence of heme oxygenase-1: the importance of neutrophils.
- Identification of a Chronic obstructive pulmonary disease genetic determinant that regulates HHIP.
- Cyclooxygenase-2 Deficiency Leads to Intestinal Barrier Dysfunction and Increased Mortality during Polymicrobial Sepsis.
- Nucleotide-Binding Oligomerization Domain Protein 2 Deficiency Enhances Neointimal Formation in Response to Vascular Injury.
- Evidence for human Lung stem cells.
- Transforming growth factor-β1 Suppression of Endotoxin-induced Heme Oxygenase-1 in macrophages involves activation of Smad2 and downregulation of Ets-2.
- Regulation of heme oxygenase-1 gene by peptidoglycan involves the interaction of Elk-1 and C/EBPalpha to increase expression.
- Distamycin A inhibits HMGA1-binding to the P-selectin promoter and attenuates Lung and liver inflammation during murine endotoxemia.
- High-mobility group box 1 contributes to lethality of endotoxemia in heme oxygenase-1-deficient mice.
- Aortic carboxypeptidase-like protein is expressed in fibrotic human Lung and its absence protects against bleomycin-induced Lung fibrosis.
- Cyclooxygenase-2 inhibition and hypoxia-induced Pulmonary hypertension: effects on Pulmonary vascular remodeling and contractility.
- Disruption of striated preferentially expressed gene locus leads to dilated cardiomyopathy in mice.
- Selective regulation of heme oxygenase-1 expression and function by insulin through IRS1/phosphoinositide 3-kinase/Akt-2 pathway.
- Absence of cyclooxygenase-2 exacerbates hypoxia-induced Pulmonary hypertension and enhances contractility of vascular smooth muscle cells.
- Heme oxygenase-1-derived carbon monoxide enhances the host defense response to microbial sepsis in mice.
- Plasma gelsolin is a marker and therapeutic agent in animal sepsis.
- The role of heme oxygenase-1 in Pulmonary disease.
- Heme oxygenase-1: a multifaceted triple-threat molecule.
- Heme oxygenase-1: a novel drug target for atherosclerotic Diseases?
- Endotoxin-induced down-regulation of Elk-3 facilitates heme oxygenase-1 induction in macrophages.
- Pathobiology of sepsis: are we still asking the same questions?
- Heme oxygenase-1 (HO-1) inhibits postmyocardial infarct remodeling and restores ventricular function.
- PU.1 regulates cathepsin S expression in professional APCs.
- Role of Ets-2 in the regulation of heme oxygenase-1 by endotoxin.
- A key role for heme oxygenase-1 in nitric oxide resistance in murine motor neurons and glia.
- Alteration in heme oxygenase-1 and nitric oxide synthase-2 gene expression during endotoxemia in cyclooxygenase-2-deficient mice.
- Reduction of nitric oxide synthase 2 expression by distamycin A improves survival from endotoxemia.
- Nitric oxide synthase-2 down-regulates surfactant protein-B expression and enhances endotoxin-induced Lung injury in mice.
- Role of HO-1 in renoprotection: location, location, location.
- Enhanced inhibition of neointimal hyperplasia by genetically engineered endothelial progenitor cells.
- Elk-3 is a transcriptional repressor of nitric-oxide synthase 2.
- Absence of heme oxygenase-1 exacerbates atherosclerotic lesion formation and vascular remodeling.
- Cyclooxygenase-2-deficient mice are resistant to endotoxin-induced inflammation and death.
- Role of heme oxygenase-1 in the regulation of blood pressure and cardiac function.
- Modulation of the thioredoxin System during inflammatory responses and its effect on heme oxygenase-1 expression.
- IFN regulatory factor-1 regulates IFN-gamma-dependent cathepsin S expression.
- Characterization of the mouse aortic carboxypeptidase-like protein promoter reveals activity in differentiated and dedifferentiated vascular smooth muscle cells.
- Gene therapy strategy for long-term myocardial protection using adeno-associated virus-mediated delivery of heme oxygenase gene.
- High-mobility group-I/Y proteins: potential role in the pathophysiology of critical illnesses.
- Heme oxygenase 1 in regulation of inflammation and oxidative damage.
- Haploinsufficiency of Hedgehog interacting protein causes increased Emphysema induced by cigarette smoke through network rewiring.
- A Chronic Obstructive Pulmonary Disease Susceptibility Gene, FAM13A, Regulates Protein Stability of β-catenin.
Schools
University Of Nebraska College Of Medicine
Mayo Clinic Mn
Procedures Preformed
- Bronchoscopy
- Ventilation Management
Conditions Treated
- Acidosis
- Asthma
- Atelectasis
- Bronchiectasis
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Doctors Specialties
- Pulmonology
Accepted Insurances
Awards
- Elected Member
Education
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Mayo School of Graduate Medical Education -
University of Nebraska College of Medicine
Hospital
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Brigham and Women's Hospital
Drug Facts
| NPI NUMBER | 1528011798 | |
| NPPES Provider LastName | PERRELLA | |
| NPPES Provider FirstName | MARK | |
| NPPES Provider ZIPCode | 021156110 | |
| NPPES Provider State | MA | |
| Specialty Description | Pulmonary Disease | |
| Total Claim Count | 38.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1528011798 |
| Last Name Of The Provider | PERRELLA |
| First Name Of The Provider | MARK |
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