The Role of Mast Cells in Stroke

Parrella, Edoardo; Porrini, Vanessa; Benarese, Marina; Pizzi, Marina

doi:10.3390/cells8050437

Cited by 45 publications

(44 citation statements)

References 207 publications

(274 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, rodent and human mast cells vary in phenotype, the immune response to stimuli, and the spectrum of mediators (pro-and anti-inflammatory) released. Thus, the findings with mast cells in rodents should also be evaluated in patients, as reported previously [13]. Mature mast cells can move from the periphery into the brain under different pathophysiological conditions [13].…”

Section: Discussionmentioning

confidence: 84%

See 1 more Smart Citation

Mast Cell Activation, Neuroinflammation, and Tight Junction Protein Derangement in Acute Traumatic Brain Injury

Kempuraj

Ahmed

Selvakumar

et al. 2020

Mediators of Inflammation

View full text Add to dashboard Cite

Traumatic brain injury (TBI) is one of the major health problems worldwide that causes death or permanent disability through primary and secondary damages in the brain. TBI causes primary brain damage and activates glial cells and immune and inflammatory cells, including mast cells in the brain associated with neuroinflammatory responses that cause secondary brain damage. Though the survival rate and the neurological deficiencies have shown significant improvement in many TBI patients with newer therapeutic options, the underlying pathophysiology of TBI-mediated neuroinflammation, neurodegeneration, and cognitive dysfunctions is understudied. In this study, we analyzed mast cells and neuroinflammation in weight drop-induced TBI. We analyzed mast cell activation by toluidine blue staining, serum chemokine C-C motif ligand 2 (CCL2) level by enzyme-linked immunosorbent assay (ELISA), and proteinase-activated receptor-2 (PAR-2), a mast cell and inflammation-associated protein, vascular endothelial growth factor receptor 2 (VEGFR2), and blood-brain barrier tight junction-associated claudin 5 and Zonula occludens-1 (ZO-1) protein expression in the brains of TBI mice. Mast cell activation and its numbers increased in the brains of 24 h and 72 h TBI when compared with sham control brains without TBI. Mouse brains after TBI show increased CCL2, PAR-2, and VEGFR2 expression and derangement of claudin 5 and ZO-1 expression as compared with sham control brains. TBI can cause mast cell activation, neuroinflammation, and derangement of tight junction proteins associated with increased BBB permeability. We suggest that inhibition of mast cell activation can suppress neuroimmune responses and glial cell activation-associated neuroinflammation and neurodegeneration in TBI.

show abstract

Section: Discussionmentioning

confidence: 84%

“…Thus, the findings with mast cells in rodents should also be evaluated in patients, as reported previously [13]. Mature mast cells can move from the periphery into the brain under different pathophysiological conditions [13].…”

Section: Discussionmentioning

confidence: 84%

Mast Cell Activation, Neuroinflammation, and Tight Junction Protein Derangement in Acute Traumatic Brain Injury

Kempuraj

Ahmed

Selvakumar

et al. 2020

Mediators of Inflammation

View full text Add to dashboard Cite

show abstract

“…Intracranial aneurysm, usually arising in the bifurcation of the cerebral artery, is the result of pathological changes that reduce the tensile strength of the arterial wall and hemodynamic blood flow to which endothelial cells are exposed [17]. It is suggested that mast cells contribute to atherosclerosis and aneurysm formation, which can exacerbate CNS (central nervous system) damage in ischemic and hemorrhagic stroke models by enhancing inflammatory responses and promoting brain-blood barrier disruption, cerebral edema, extravasation, and SAH [18,19]. Moreover, an increase in the level of macrophages, T-lymphocytes, and leukocytes in the wall leads to increased production of ROS, which can modify proteins and lipids, including LDLs (low density lipoproteins), causing atherosclerotic changes in the walls of the vessels.…”

Section: Discussionmentioning

confidence: 99%

Clinical Prognosis for SAH Consistent with Redox Imbalance and Lipid Peroxidation

et al. 2020

View full text Add to dashboard Cite

Subarachnoid hemorrhage (SAH) accounts for 3% of all strokes. As more and more data indicates the role of oxidative stress in acute brain damage caused by SAH, an attempt was made to correlate the clinical status of patients with systemic level of antioxidants and lipid peroxidation products. The hemorrhage was diagnosed with brain computed tomography (CT) and aneurysm with angio-CT and angiography, while the vasospasm was monitored with transcranial Doppler. Plasma glutathione peroxidase activity (GSH-Px) and vitamin A, E, and C levels were determined spectrophotometrically and by HPLC, respectively. The levels of polyunsaturated fatty acids (PUFAs) cyclization products were determined by GC-MS, while F 2 -isoprostanes and neuroprostanes (NP) were determined by LC-MS. SAH was accompanied by changes in antioxidant capacity in blood plasma, including initially (day 1) an increase in GSH-Px activity, followed by its decrease and a progressive decrease in glutathione (GSH) levels and vitamins A, E, and C. On the other hand, levels of PUFAs cyclization products, F 2 -isoprostanes, and neuroprostanes were highest on day 1 (two and eight times higher, respectively) and decreased over time. The levels of 4-HNE (4-hydroxynonenal), 4-ONE (4-oxononenal), and MDA (malondialdehyde) changed similarly. In contrast, the 4-HHE (4-hydroxyhexenal) level reduced after SAH increased significantly after a week. It was found that the deterioration of the overall clinical and neurological condition of SAH patients due to cerebral edema, intracranial hemorrhage, or vasoconstriction corresponded to reduced antioxidant defense and, as a consequence, increased lipid peroxidation and slower observed changes in regression. It can be concluded that monitoring the level of lipid peroxidation products (neuroprostanes, 4-ONE, and MDA) can support the monitoring of the clinical status of patients, especially with regard to the assessment of vasospasm.

show abstract

“…Pseudo‐allergic reaction could be immediately triggered when contacted with the allergen at the first time and induced a hypersensitivity‐like pathological symptom, such as skin rash, tissue oedema and asthmatic response . Mast cells are the key mediate of allergy and play an important role in the acute hypersensitivity . The laboratory of allergic disease 2 (LAD2) cell line was a kind of human primary mast cell that was always used as response cells in the in vitro allergic reaction study .…”

Section: Introductionmentioning

confidence: 99%

Discovery and analysis the anti-pseudo-allergic components from Perilla frutescens leaves by overexpressed MRGPRX2 cell membrane chromatography coupled with HPLC-ESI-IT-TOF system

Yang

Zeng

Wang

et al. 2020

Journal of Pharmacy and Pharmacology

View full text Add to dashboard Cite

Objectives Screen and identify the anti-pseudo-allergic activity components of Perilla frutescens leaves that interacted with MRGPRX2 (a new reported pseudoallergic reaction-related receptor). Methods An overexpressed MRGPRX2 cell membrane chromatography (CMC) coupled with HPLC-ESI-IT-TOF system has been established to screen and identify the effective components from P. frutescens leaves. A frontal analysis method was performed to investigate the binding affinity between ligands and MRGPRX2. Their activity of relieving pseudo-allergic reaction was evaluated in vitro by histamine release assay, β-hexosaminidase release assay and intracellular Ca 2+ mobilization assay. Key findings Extract of P. frutescens leaves was proved to be effective in antipseudo-allergic reaction by inhibiting MRGPRX2. Apigenin (API) and rosmarinic acid (ROS) were confirmed to be the potential anti-allergy compounds that could bind with MRGPRX2. The binding affinity (K D ) of ROS and API with MRGPRX2 was (8.79 ± 0.13) 9 10 −8 M and (6.54 ± 1.69) 9 10 −8 M, respectively. The IC 50 of API inhibiting laboratory of allergic disease 2 cells degranulation was also determined to be (51.96 ± 0.18) μM. Conclusions A MRGPRX2/CMC coupled with HPLC-ESI-IT-TOF system was successfully established and applied to discover the effective components from P. frutescens leaves.

show abstract

The Role of Mast Cells in Stroke

Cited by 45 publications

References 207 publications

Mast Cell Activation, Neuroinflammation, and Tight Junction Protein Derangement in Acute Traumatic Brain Injury

Mast Cell Activation, Neuroinflammation, and Tight Junction Protein Derangement in Acute Traumatic Brain Injury

Clinical Prognosis for SAH Consistent with Redox Imbalance and Lipid Peroxidation

Discovery and analysis the anti-pseudo-allergic components from Perilla frutescens leaves by overexpressed MRGPRX2 cell membrane chromatography coupled with HPLC-ESI-IT-TOF system

Contact Info

Product

Resources

About