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Article: Molecular Mechanisms of Vascular Damage During Lung Injury.

Bossardi Ramos, Ramon / Adam, Alejandro Pablo

Advances in experimental medicine and biology

2021 Volume 1304, Page(s) 95–107

Abstract: A variety of pulmonary and systemic insults promote an inflammatory response causing increased vascular permeability, leading to the development of acute lung injury (ALI), a condition necessitating hospitalization and intensive care, or the more severe ... ...

Abstract	A variety of pulmonary and systemic insults promote an inflammatory response causing increased vascular permeability, leading to the development of acute lung injury (ALI), a condition necessitating hospitalization and intensive care, or the more severe acute respiratory distress syndrome (ARDS), a disease with a high mortality rate. Further, COVID-19 pandemic-associated ARDS is now a major cause of mortality worldwide. The pathogenesis of ALI is explained by injury to both the vascular endothelium and the alveolar epithelium. The disruption of the lung endothelial and epithelial barriers occurs in response to both systemic and local production of pro-inflammatory cytokines. Studies that evaluate the association of genetic polymorphisms with disease risk did not yield many potential therapeutic targets to treat and revert lung injury. This failure is probably due in part to the phenotypic complexity of ALI/ARDS, and genetic predisposition may be obscured by the multiple environmental and behavioral risk factors. In the last decade, new research has uncovered novel epigenetic mechanisms that control ALI/ARDS pathogenesis, including histone modifications and DNA methylation. Enzyme inhibitors such as DNMTi and HDACi may offer new alternative strategies to prevent or reverse the vascular damage that occurs during lung injury. This review will focus on the latest findings on the molecular mechanisms of vascular damage in ALI/ARDS, the genetic factors that might contribute to the susceptibility for developing this disease, and the epigenetic changes observed in humans, as well as in experimental models of ALI/ADRS.
MeSH term(s)	Acute Lung Injury/genetics ; COVID-19 ; Humans ; Lung ; Pandemics ; Respiratory Distress Syndrome/genetics ; SARS-CoV-2
Language	English
Publishing date	2021-01-01
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-3-030-68748-9_6
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Article: A transient brain endothelial translatome response to endotoxin is associated with mild cognitive changes post-shock in young mice.

Lu, Shuhan / Portela, Iria Di John / Martino, Nina / Ramos, Ramon Bossardi / Salinero, Abigail E / Smith, Rachel M / Zuloaga, Kristen L / Adam, Alejandro P

bioRxiv : the preprint server for biology

2024

Abstract: Sepsis-associated encephalopathy (SAE) is a common manifestation in septic patients that is associated with increased risk of long-term cognitive impairment. SAE is driven, at least in part, by brain endothelial dysfunction in response to systemic ... ...

Abstract	Sepsis-associated encephalopathy (SAE) is a common manifestation in septic patients that is associated with increased risk of long-term cognitive impairment. SAE is driven, at least in part, by brain endothelial dysfunction in response to systemic cytokine signaling. However, the mechanisms driving SAE and its consequences remain largely unknown. Here, we performed translating ribosome affinity purification (TRAP) and RNA-sequencing (TRAP-seq) from the brain endothelium to determine the transcriptional changes after an acute endotoxemic (LPS) challenge. We found that LPS induces a strong acute transcriptional response in the brain endothelium that partially correlates with the whole brain transcriptional response and suggested an endothelial-specific hypoxia response. Consistent with a critical role for the IL-6 pathway, loss of the main regulator of this pathway, SOCS3, leads to a broadening of the population of genes responsive to LPS, suggesting that an overactivation of the IL-6/JAK/STAT3 pathway leads to an increased transcriptional response that could explain our prior findings of severe brain injury in these mice. To identify any potential sequelae of this acute response, we performed brain TRAP-seq following a battery of behavioral tests in mice after apparent recovery. We found that the transcriptional response returns to baseline within days post-challenge. Despite the transient nature of the response, we observed that mice that recovered from the endotoxemic shock showed mild, sex-dependent cognitive impairment, suggesting that the acute brain injury led to sustained, non-transcriptional effects. A better understanding of the transcriptional and non-transcriptional changes in response to shock is needed in order to prevent and/or revert the devastating consequences of septic shock.
Language	English
Publishing date	2024-03-06
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.03.03.583191
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Article ; Online: SOCS3 limits TNF and endotoxin-induced endothelial dysfunction by blocking a required autocrine interleukin-6 signal in human endothelial cells.

Martino, Nina / Bossardi Ramos, Ramon / Chuy, Dareen / Tomaszek, Lindsay / Adam, Alejandro P

American journal of physiology. Cell physiology

2022 Volume 323, Issue 2, Page(s) C556–C569

Abstract: Increased circulating levels of soluble interleukin (IL)-6 receptor α (sIL-6Rα) are commonly observed during inflammatory responses, allowing for IL-6 signaling in cells that express the ubiquitous receptor subunit gp130 but not IL-6Rα, such as ... ...

Abstract	Increased circulating levels of soluble interleukin (IL)-6 receptor α (sIL-6Rα) are commonly observed during inflammatory responses, allowing for IL-6 signaling in cells that express the ubiquitous receptor subunit gp130 but not IL-6Rα, such as endothelial cells. Activation of Toll-like receptor (TLR)-4 or the tumor necrosis factor (TNF) receptor leads to NF-κB-dependent increases in endothelial IL-6 expression. Thus, we hypothesize that danger signals may induce autocrine IL-6 signaling within the endothelium via sIL-6Rα-mediated trans-signaling. In support of this hypothesis, we recently demonstrated that conditional deletion in the endothelium of the IL-6 signaling inhibitor SOCS3 leads to rapid mortality in mice challenged with the TLR-4 agonist endotoxin through increases in vascular leakage, thrombosis, leukocyte adhesion, and a type I-like interferon response. Here, we sought to directly test a role for sIL-6Rα in LPS-treated human umbilical vein and dermal blood microvascular endothelial cells. We show that cotreatment with sIL-6Rα dramatically increases the loss of barrier function and the expression of COX2 and tissue factor mRNA levels induced by LPS. This cotreatment led to strong activation of STAT1 and STAT3 while not affecting LPS-induced activation of p38 and NF-κB signaling. Similar results were obtained when sIL-6Rα was added to a TNF challenge. JAK inhibition by pretreatment with ruxolitinib or by SOCS3 overexpression blunted LPS and sIL-6R synergistic effects, whereas SOCS3 knockdown further increased the response. Together, these findings demonstrate that IL-6 signaling downstream of NF-κB activation leads to a strong endothelial activation and may explain the acute endotheliopathy observed during critical illness.
MeSH term(s)	Animals ; Endothelial Cells/metabolism ; Endothelium/metabolism ; Endotoxins/metabolism ; Endotoxins/toxicity ; Humans ; Interleukin-6/metabolism ; Lipopolysaccharides/toxicity ; Mice ; NF-kappa B/metabolism ; Suppressor of Cytokine Signaling 3 Protein/genetics ; Suppressor of Cytokine Signaling 3 Protein/metabolism ; Suppressor of Cytokine Signaling Proteins/metabolism
Chemical Substances	Endotoxins ; Interleukin-6 ; Lipopolysaccharides ; NF-kappa B ; SOCS3 protein, human ; Socs3 protein, mouse ; Suppressor of Cytokine Signaling 3 Protein ; Suppressor of Cytokine Signaling Proteins
Language	English
Publishing date	2022-07-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00171.2022
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Article: Metabolic Features of Women With Polycystic Ovary Syndrome in Latin America: A Systematic Review.

Marchesan, Lucas Bandeira / Ramos, Ramon Bossardi / Spritzer, Poli Mara

Frontiers in endocrinology

2021 Volume 12, Page(s) 759835

Abstract: Background: Polycystic ovary syndrome (PCOS) is an endocrine disorder that commonly affects women of childbearing age and has been associated with metabolic and reproductive abnormalities. Only a few studies have investigated metabolic traits in women ... ...

Abstract	Background: Polycystic ovary syndrome (PCOS) is an endocrine disorder that commonly affects women of childbearing age and has been associated with metabolic and reproductive abnormalities. Only a few studies have investigated metabolic traits in women with PCOS in Latin America. Therefore, we conducted a systematic review to provide an overview of the available evidence on the metabolic profile of Latin American women with PCOS. Methods: We searched PubMed, Cochrane Central Register of Controlled Trials, and Embase databases for cross-sectional, case-control, or cohort studies focusing on populations of countries in South and Central America and Mexico, published until October 31, 2019. We selected studies that reported the diagnostic criteria for PCOS. In the absence of a control group, we included studies if they reported relevant metabolic data. Results: The initial search yielded 4878 records, of which 41 studies were included in the systematic review. Sample sizes ranged from 10 to 288 in PCOS groups and from 10 to 1500 in control groups. The prevalence of phenotypes A and B (classic PCOS) ranged from 65.8% to 87.5% as reported in studies from Argentina, Brazil, and Chile. Metabolic syndrome ranged from 33.3% to 44.0% for phenotype A, from 15.0% to 58.0% for phenotype B, from 11.9% to 36.0% for phenotype C, and from 14.2% to 66.0% for phenotype D. Women with PCOS had higher body mass index, waist circumference, blood pressure, glucose, and homeostasis model assessment index as well as a more adverse lipid profile than those without PCOS. Conclusions: Evidence from the present systematic review suggests that anthropometric and metabolic profiles are worse in women with PCOS who live in different Latin American countries than in women without PCOS living in the same region. Additional studies assessing metabolic comorbidities, such as diabetes, and distinct PCOS phenotypes in different Latin American countries are warranted and may produce invaluable information for primary and secondary prevention of PCOS in the region. This systematic review was registered with PROSPERO under number CRD42016038537. Systematic review registration: PROSPERO, identifier CRD42016038537.
MeSH term(s)	Female ; Humans ; Latin America/epidemiology ; Polycystic Ovary Syndrome/epidemiology ; Polycystic Ovary Syndrome/metabolism
Language	English
Publishing date	2021-10-19
Publishing country	Switzerland
Document type	Research Support, Non-U.S. Gov't ; Systematic Review
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2021.759835
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Article ; Online: SH2 domain-containing protein tyrosine phosphatase-2 is enriched in eyelid specimens of rosacea.

Chebolu, Apoorv / Ramos, Ramon Bossardi / Arunachalam, Thilaka / Adam, Alejandro Pablo / Wladis, Edward J

Skin health and disease

2022 Volume 3, Issue 1, Page(s) e190

Abstract: Background: Rosacea is a cutaneous disease that may secondarily affect the ocular surface. Due to the vision threatening, cosmetic, psychological, and work productivity impact, the identification of cellular targets that govern rosacea would enhance our ...

Abstract	Background: Rosacea is a cutaneous disease that may secondarily affect the ocular surface. Due to the vision threatening, cosmetic, psychological, and work productivity impact, the identification of cellular targets that govern rosacea would enhance our understanding of the biology of the disease and delineate targets for therapeutic manipulation. Objective: To characterize the involvement of SH2 domain-containing protein tyrosine phosphatase-2 (SHP2) in the pathogenesis of rosacea. Methods: Specimens from elective ectropion surgery ( Results: On WB, SHP2 was expressed in higher concentrations in rosacea specimens ( Conclusions: SHP2 is enriched in cutaneous specimens of rosacea, suggesting a critical role for this protein in the disease and indicating a modifiable therapeutic moiety.
Language	English
Publishing date	2022-11-17
Publishing country	England
Document type	Journal Article
ISSN	2690-442X
ISSN (online)	2690-442X
DOI	10.1002/ski2.190
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Article: The Effect of Gender-Affirming Hormone Therapy on the Risk of Subclinical Atherosclerosis in the Transgender Population: A Systematic Review.

Moreira Allgayer, Roberta M C / Borba, Gustavo da Silva / Moraes, Ruy Silveira / Ramos, Ramon Bossardi / Spritzer, Poli Mara

Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists

2023 Volume 29, Issue 6, Page(s) 498–507

Abstract: Objective: The impact of gender-affirming hormone therapy (GAHT) on cardiovascular (CV) health is still not entirely established. A systematic review was conducted to summarize the evidence on the risk of subclinical atherosclerosis in transgender ... ...

Abstract	Objective: The impact of gender-affirming hormone therapy (GAHT) on cardiovascular (CV) health is still not entirely established. A systematic review was conducted to summarize the evidence on the risk of subclinical atherosclerosis in transgender people receiving GAHT. Methods: A systematic review was performed following Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines, and data were searched in PubMed, LILACS, EMBASE, and Scopus databases for cohort, case-control, and cross-sectional studies or randomized clinical trials, including transgender people receiving GAHT. Transgender men and women before and during/after GAHT for at least 2 months, compared with cisgender men and women or hormonally untreated transgender persons. Studies reporting changes in variables related to endothelial function, arterial stiffness, autonomic function, and blood markers of inflammation/coagulation associated with CV risk were included. Results: From 159 potentially eligible studies initially identified, 12 were included in the systematic review (8 cross-sectional and 4 cohort studies). Studies of trans men receiving GAHT reported increased carotid thickness, brachial-ankle pulse wave velocity, and decreased vasodilation. Studies of trans women receiving GAHT reported decreased interleukin 6, plasminogen activator inhibitor-1, and tissue plasminogen activator levels and brachial-ankle pulse wave velocity, with variations in flow-mediated dilation and arterial stiffness depending on the type of treatment and route of administration. Conclusions: The results suggest that GAHT is associated with an increased risk of subclinical atherosclerosis in transgender men but may have either neutral or beneficial effects in transgender women. The evidence produced is not entirely conclusive, suggesting that additional studies are warranted in the context of primary prevention of CV disease in the transgender population receiving GAHT. Systematic review registration: PROSPERO, identifier CRD42022323757.
MeSH term(s)	Male ; Female ; Humans ; Transgender Persons ; Tissue Plasminogen Activator ; Ankle Brachial Index ; Cross-Sectional Studies ; Pulse Wave Analysis ; Atherosclerosis/epidemiology ; Atherosclerosis/prevention & control ; Hormones
Chemical Substances	Tissue Plasminogen Activator (EC 3.4.21.68) ; Hormones
Language	English
Publishing date	2023-01-02
Publishing country	United States
Document type	Systematic Review ; Journal Article ; Review
ZDB-ID	1473503-9
ISSN	1530-891X
ISSN	1530-891X
DOI	10.1016/j.eprac.2022.12.017
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Article ; Online: DMT1-dependent endosome-mitochondria interactions regulate mitochondrial iron translocation and metastatic outgrowth.

Barra, Jonathan / Crosbourne, Isaiah / Roberge, Cassandra L / Bossardi-Ramos, Ramon / Warren, Janine S A / Matteson, Kailie / Wang, Ling / Jourd'heuil, Frances / Borisov, Sergey M / Bresnahan, Erin / Bravo-Cordero, Jose Javier / Dmitriev, Ruslan I / Jourd'heuil, David / Adam, Alejandro P / Lamar, John M / Corr, David T / Barroso, Margarida M

Oncogene

2024 Volume 43, Issue 9, Page(s) 650–667

Abstract: Transient early endosome (EE)-mitochondria interactions can mediate mitochondrial iron translocation, but the associated mechanisms are still elusive. We showed that Divalent Metal Transporter 1 (DMT1) sustains mitochondrial iron translocation via EE- ... ...

Abstract	Transient early endosome (EE)-mitochondria interactions can mediate mitochondrial iron translocation, but the associated mechanisms are still elusive. We showed that Divalent Metal Transporter 1 (DMT1) sustains mitochondrial iron translocation via EE-mitochondria interactions in triple-negative MDA-MB-231, but not in luminal A T47D breast cancer cells. DMT1 silencing increases labile iron pool (LIP) levels and activates PINK1/Parkin-dependent mitophagy in MDA-MB-231 cells. Mitochondrial bioenergetics and the iron-associated protein profile were altered by DMT1 silencing and rescued by DMT1 re-expression. Transcriptomic profiles upon DMT1 silencing are strikingly different between 2D and 3D culture conditions, suggesting that the environment context is crucial for the DMT1 knockout phenotype observed in MDA-MB-231 cells. Lastly, in vivo lung metastasis assay revealed that DMT1 silencing promoted the outgrowth of lung metastatic nodules in both human and murine models of triple-negative breast cancer cells. These findings reveal a DMT1-dependent pathway connecting EE-mitochondria interactions to mitochondrial iron translocation and metastatic fitness of breast cancer cells.
MeSH term(s)	Animals ; Female ; Humans ; Mice ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Endosomes/metabolism ; Iron/metabolism ; Mitochondria/metabolism ; Mitophagy
Chemical Substances	Iron (E1UOL152H7) ; DMRT1 protein
Language	English
Publishing date	2024-01-06
Publishing country	England
Document type	Journal Article
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-023-02933-x
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Article: Metabolic profile of women with PCOS in Brazil: a systematic review and meta-analysis.

Spritzer, Poli Mara / Ramos, Ramon Bossardi / Marchesan, Lucas Bandeira / de Oliveira, Monica / Carmina, Enrico

Diabetology & metabolic syndrome

2021 Volume 13, Issue 1, Page(s) 18

Abstract: Background: Polycystic ovary syndrome (PCOS) is a common endocrine disease affecting women of reproductive age and associated with reproductive and metabolic dysfunction. Few studies are available regarding metabolic traits in Brazilian women with PCOS. ...

Abstract	Background: Polycystic ovary syndrome (PCOS) is a common endocrine disease affecting women of reproductive age and associated with reproductive and metabolic dysfunction. Few studies are available regarding metabolic traits in Brazilian women with PCOS. The aim of this systematic review and meta-analysis was to summarize the available evidence regarding metabolic traits and comorbidities in Brazilian women with polycystic ovary syndrome (PCOS). Methods: We systematically searched PubMed, Cochrane Central Register of Controlled Trials, and Embase for cross-sectional, case-control, or cohort studies focusing on populations of different regions from Brazil, published until July 31, 2019. Studies were selected if they reported PCOS diagnostic criteria. Studies without a control group were included if they presented relevant metabolic data. Results: Of 4856 studies initially identified, 27 were included in the systematic review and 12 were included in the meta-analysis, for a total of 995 women with PCOS defined by Rotterdam criteria and 2275 controls from different regions of Brazil. Obesity, metabolic syndrome and IGT were prevalent, and standard mean differences for BMI (SMD 0.67, 95% CI, 0.29, 1.05), waist circumference (SMD 0.22, 95% CI 0.02, 0.41), systolic (SMD 0.66, 95% CI 0.30, 1.01) and diastolic blood pressure (SMD 0.55, 95% CI 0.24, 0.87), glucose (SMD 0.21, 95% CI 0.04, 0.38) and HOMA (SMD 0.78, 95% CI 0.52, 1.04) were significantly higher in Brazilian women with PCOS compared to controls. Lipid profile was more adverse in PCOS vs. non-PCOS women. Between-study heterogeneities were low/moderate for glucose and HOMA and moderate/high for the other variables. Conclusions: The data of this systematic review and meta-analysis indicate that Brazilian women with PCOS have a worse metabolic profile than women without PCOS with no important regional differences. The prevalence of metabolic changes is intermediate in Brazil vs. other countries.
Language	English
Publishing date	2021-02-16
Publishing country	England
Document type	Journal Article
ZDB-ID	2518786-7
ISSN	1758-5996
ISSN	1758-5996
DOI	10.1186/s13098-021-00636-5
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Article ; Online: Shock drives a STAT3 and JunB-mediated coordinated transcriptional and DNA methylation response in the endothelium.

Ramos, Ramon Bossardi / Martino, Nina / Chuy, Dareen / Lu, Shuhan / Zuo, Mei Xing G / Balasubramanian, Uma / Di John Portela, Iria / Vincent, Peter A / Adam, Alejandro P

Journal of cell science

2023 Volume 136, Issue 18

Abstract: Endothelial dysfunction is a crucial factor in promoting organ failure during septic shock. However, the underlying mechanisms are unknown. Here, we show that kidney injury after lipopolysaccharide (LPS) insult leads to strong endothelial transcriptional ...

Abstract	Endothelial dysfunction is a crucial factor in promoting organ failure during septic shock. However, the underlying mechanisms are unknown. Here, we show that kidney injury after lipopolysaccharide (LPS) insult leads to strong endothelial transcriptional and epigenetic responses. Furthermore, SOCS3 loss leads to an aggravation of the responses, demonstrating a causal role for the STAT3-SOCS3 signaling axis in the acute endothelial response to LPS. Experiments in cultured endothelial cells demonstrate that IL-6 mediates this response. Furthermore, bioinformatics analysis of in vivo and in vitro transcriptomics and epigenetics suggests a role for STAT, AP1 and interferon regulatory family (IRF) transcription factors. Knockdown of STAT3 or the AP1 member JunB partially prevents the changes in gene expression, demonstrating a role for these transcription factors. In conclusion, endothelial cells respond with a coordinated response that depends on overactivated IL-6 signaling via STAT3, JunB and possibly other transcription factors. Our findings provide evidence for a critical role of IL-6 signaling in regulating shock-induced epigenetic changes and sustained endothelial activation, offering a new therapeutic target to limit vascular dysfunction.
MeSH term(s)	DNA Methylation/genetics ; Endothelial Cells ; Interleukin-6/genetics ; Lipopolysaccharides ; Endothelium
Chemical Substances	Interleukin-6 ; Lipopolysaccharides
Language	English
Publishing date	2023-09-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2993-2
ISSN	1477-9137 ; 0021-9533
ISSN (online)	1477-9137
ISSN	0021-9533
DOI	10.1242/jcs.261323
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Article ; Online: First-year students’ perceptions of team-based learning in a new medical genetics course

Vinicius Canato Santana / Carlos Rocha Oliveira / Ramon Bossardi Ramos

Revista Brasileira de Educação Médica, Vol 43, Iss 3, Pp 170-

2019 Volume 177

Abstract: ABSTRACT Background Medical education has evolved considerably over the last few years, especially through adoption of new technologies and active methodologies. These methodologies aim to improve learning and engage students deeply in the process. TBL ... ...

Abstract	ABSTRACT Background Medical education has evolved considerably over the last few years, especially through adoption of new technologies and active methodologies. These methodologies aim to improve learning and engage students deeply in the process. TBL is a methodology widely used in health schools, including Medical Schools. We can use it to work with large groups, divided into small teams. The students first work individually, then within teams, and finally the groups cooperate to solve applied problems. Objectives To describe students’ perceptions and satisfaction about a Medical Genetics course organized into blocks of subject in which we used TBL sessions with first-year medical students. Methods A Medical Genetics course were organized into subject blocks in which a TBL session was conducted in each of these blocks to improve the learning process. At the end of the course, the students answered a questionnaire on satisfaction and perceptions. Results By the first time we described a Medical Genetics course organized into 5 blocks of subject matter on a total of 25 genetic diseases in which a TBL session was conducted in each of these blocks. We enrolled a total of 290 participants and 96% of the students were satisfied with TBL. Furthermore, 97% of students believe that TBL helped them to learn, and 87% approved of use of TBL in the future at other stages of their medical course. Conclusion Application of the TBL method during a medical genetics course was well-received by students and proved an important tool in the structures of curricula for medical education at this university.
Keywords	–Active learning ; –Medical Genetics ; Education (General) ; L7-991 ; Medicine (General) ; R5-920
Subject code	370
Language	Portuguese
Publishing date	2019-05-01T00:00:00Z
Publisher	Associção Brasileira de Educação Médica
Document type	Article ; Online
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