Tissue Inhibitor of Matrix Metalloproteinases-1 (TIMP-1) and Pulmonary Involvement in COVID-19 Pneumonia

Zingaropoli, Maria Antonella; Latronico, Tiziana; Pasculli, Patrizia; Masci, Giorgio Maria; Merz, Rachel; Ciccone, Federica; Dominelli, Federica; Borgo, Cosmo Del; Lichtner, Miriam; Iafrate, Franco; Galardo, Gioacchino; Pugliese, Francesco; Panebianco, Valeria; Ricci, Paolo; Catalano, Carlo; Ciardi, Maria Rosa; Liuzzi, Grazia Maria; Mastroianni, Claudio Maria

doi:10.3390/biom13071040

Cited by 5 publications

(2 citation statements)

References 74 publications

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“…Specifically, at the Department of Public Health and Infectious Diseases, Policlinico Umberto I, Sapienza, University of Rome, (baseline) adult patients (≥18 years old) were enrolled upon hospital admission. As previously described [ 45 , 46 ], COVID-19-related pneumonia was diagnosed by high-resolution chest computed tomography (CT) scan associated with SARS-CoV-2 RNA detection from a nasopharyngeal swab through a commercial reverse transcription-polymerase chain reaction (RT-PCR) kit, following manufacturer’s instructions (RealStar ® SARS-CoV-2 Altona Diagnostic, Hamburg, Germany).…”

Section: Methodsmentioning

confidence: 99%

Biomarkers of Neurological Damage: From Acute Stage to Post-Acute Sequelae of COVID-19

Zingaropoli,

Pasculli,

Barbato

et al. 2023

Cells

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Neurological symptoms (NS) in COVID-19 are related to both acute stage and long-COVID. We explored levels of brain injury biomarkers (NfL and GFAP) and myeloid activation marker (sCD163) and their implications on the CNS. Materials and Methods: In hospitalized COVID-19 patients plasma samples were collected at two time points: on hospital admission (baseline) and three months after hospital discharge (Tpost). Patients were stratified according to COVID-19 severity based on acute respiratory distress syndrome (ARDS) onset (severe and non-severe groups). A further stratification according to the presence of NS (with and without groups) at baseline (requiring a puncture lumbar for diagnostic purposes) and according to NS self-referred at Tpost was performed. Finally, cerebrospinal fluid (CSF) samples were collected from patients with NS present at baseline. Results: We enrolled 144 COVID-19 patients (62 female/82 male; median age [interquartile range, IQR]): 64 [55,56,57,58,59,60,61,62,63,64,65,66,67,68,69,70,71,72,73,74,75,76,77]) and 53 heathy donors (HD, 30 female/23 male; median age [IQR]: 64 [59,60,61,62,63,64,65,66,67,68,69]). At baseline, higher plasma levels of NfL, GFAP and sCD163 in COVID-19 patients compared to HD were observed (p < 0.0001, p < 0.0001 and p < 0.0001, respectively), especially in those with severe COVID-19 (p < 0.0001, p < 0.0001 and p < 0.0001, respectively). Patients with NS showed higher plasma levels of NfL, GFAP and sCD163 compared to those without (p = 0.0023, p < 0.0001 and 0.0370, respectively). At baseline, in COVID-19 patients with NS, positive correlations between CSF levels of sCD163 and CSF levels of NfL (ρ = 0.7536, p = 0.0017) and GFAP were observed (ρ = 0.7036, p = 0.0045). At Tpost, the longitudinal evaluation performed on 77 COVID-19 patients showed a significant reduction in plasma levels of NfL, GFAP and sCD163 compared to baseline (p < 0.0001, p < 0.0001 and p = 0.0413, respectively). Finally, at Tpost, in the severe group, higher plasma levels of sCD163 in patients with NS compared to those without were reported (p < 0.0001). Conclusions: High plasma levels of NfL, GFAP and sCD163 could be due to a proinflammatory systemic and brain response involving microglial activation and subsequent CNS damage. Our data highlight the association between myeloid activation and CNS perturbations.

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Section: Methodsmentioning

confidence: 99%

Biomarkers of Neurological Damage: From Acute Stage to Post-Acute Sequelae of COVID-19

Zingaropoli,

Pasculli,

Barbato

et al. 2023

Cells

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“…MMPs participate in several physiological processes including embryonic development, coagulation cascade and fibrinolysis, as well as in pathological processes such as lung diseases, vascular changes, obesity, inflammation, cancer and atherosclerosis [108][109][110][111][112][113]. More recently, these enzymes were also associated with clinical manifestations during coronavirus infection [114][115][116].…”

Section: Mmp-2 Mmp-9mentioning

confidence: 99%

The Role of Platelet Molecules in Risk Stratification of Patients with COVID-19

de Oliveira Sales,

de Oliveira,

da Silva

et al. 2023

Hemato

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The new severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was first reported in China and is responsible for Coronavirus disease (COVID-19). Despite being well tolerated by most patients, a fraction of cases evolve into a potentially fatal condition requiring intensive care. In addition to respiratory complications, several studies have reported cases of patients who developed intense thrombosis, including acute myocardial infarction and ischemic stroke, as well as the presence of elevated coagulation markers. Evidence has shown that the virus can interact directly with platelets and modulate their thrombotic and inflammatory functions, with significant prognostic implications. It is important to highlight that the emerging literature shows that when hyperactive these cells can act as pro-viral infections both in transporting their particles and in increasing inflammation, leading to a hyperinflammatory state and consequent clinical worsening. In this review, we searched for studies available in public databases and discussed the interaction of platelet biomarkers in the pathogenesis of COVID-19. In this context, understanding the mechanism of SARS-CoV-2 and these cells in different clinical conditions could help us to understand the coagulation and inflammation profiles of critically ill patients with the disease, guiding faster clinical management and enabling the reuse and targeting of more efficient therapies.

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The TIMP protein family: diverse roles in pathophysiology

Coates-Park,

Rich,

Stetler-Stevenson

et al. 2024

American Journal of Physiology-Cell Physiology

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The Tissue Inhibitors of Matrix Metalloproteinases (TIMPs) are a family of four matrisome proteins classically defined by their roles as the primary endogenous inhibitors of Metalloproteinases (MPs). Their functions however are not limited to MP-inhibition, with each family member harboring numerous MP-independent biological functions that play key roles in processes such as inflammation and apoptosis. Because of these multifaceted functions, TIMPs have been cited in diverse pathophysiological contexts. Herein we provide a comprehensive overview of the MP-dependent and -independent roles of TIMPs across a range of pathological conditions. The potential therapeutic and biomarker applications of TIMPs in these disease contexts are also considered, highlighting the biomedical promise of this complex and often misunderstood protein family.

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Tissue Inhibitor of Matrix Metalloproteinases-1 (TIMP-1) and Pulmonary Involvement in COVID-19 Pneumonia

Cited by 5 publications

References 74 publications

Biomarkers of Neurological Damage: From Acute Stage to Post-Acute Sequelae of COVID-19

Biomarkers of Neurological Damage: From Acute Stage to Post-Acute Sequelae of COVID-19

The Role of Platelet Molecules in Risk Stratification of Patients with COVID-19

The TIMP protein family: diverse roles in pathophysiology

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