Galectins in inflammatory skin diseases: current roles and future directions.

Galectins (LGALS) are β-galactoside-binding lectins involved in immune regulation, epithelial integrity, and tissue remodeling. In the skin, they exhibit cell type-specific expression across keratinocytes, fibroblasts, and immune cells, shaping inflammatory signaling and barrier homeostasis. In this review, we examine LGALS expression and function in inflammatory skin diseases, with a focus on atopic dermatitis (AD) and psoriasis (Pso).

Ac Hydrogel Modulates IL-1β-Driven Inflammation via Mast Cell-Associated and Immune Regulatory Pathways in Diabetic Wounds.

Chronic, non-resolving inflammation is a major contributor to impaired wound healing in diabetes. Annexin A1 (AnxA1), a pro-resolving mediator, and its mimetic peptide Ac have demonstrated therapeutic potential in modulating inflammatory responses. In this study, we evaluated the effects of topical Ac hydrogel in a streptozotocin-induced diabetic wound model.

Spatial immune profiling reveals distinct microenvironments in medullary thyroid carcinoma.

Introduction: Medullary thyroid carcinoma (MTC) is a rare and aggressive thyroid cancer with a challenging prognosis. While the immune microenvironment plays a crucial role in cancer progression, its role in MTC remains underexplored compared to more common thyroid cancers.

Methods: this study investigates the immune landscape of MTC by systematically evaluating immune cell infiltration and expression of immune markers across various tissue topographies.

Functional role of Annexin A1 and S100A11 in psoriasis pathogenesis: Insights from IMQ-induced models and keratinocyte modulation.

Psoriasis (Pso) is a chronic inflammatory skin disease involving immune dysregulation and epidermal hyperplasia. Annexin A1 (ANXA1), a glucocorticoid-regulated protein, and S100A11 are implicated in keratinocyte function, but their roles in Pso remain unclear. This study translationally elucidates the functional role of ANXA1 and S100A11 in Pso by integrating analyses in human and murine skin biopsies and in vitro assays using human keratinocytes.

Exploring the therapeutic potential of annexin A1-derived peptide Ac in modulating NLRP3 inflammasome activation in Crohn's disease.

Inflammatory bowel disease (IBD) remains a complex and multifaceted condition, with its management dependent on a thorough understanding of its underlying mechanisms. While the ANXA1-FPR axis is implicated in the pathogenesis of IBD, its relationship with the NLRP3 inflammasome in this context has not been established. Thus, this study aimed to elucidate the intricate relationship between ANXA1, FPRs, and the NLRP3 inflammasome in the pathogenesis of IBD.

Botulinum Toxin Type A: Is It Really Useful in Improving the Aesthetic Results of Extrafacial Scars? A Prospective, Randomized, Double-Blinded Study.

Background: The role of botulinum toxin type A (BoNTA) in scar prevention has been studied mainly in facial and cervical regions, but its effects on extrafacial scars remain unclear. This study evaluated BoNTA's impact on scar aesthetics and its potential modulation of the NLRP3 inflammasome in wounds on the back.

Methods: A prospective, double-blind, randomized controlled trial was conducted with 23 participants undergoing fusiform excision of benign skin lesions.

Regulatory role of annexin A1 in NLRP3 inflammasome activation in atopic dermatitis: insights from keratinocytes in human and murine studies.

Despite the well-documented regulatory role of annexin A1 (ANXA1) in numerous stages of the inflammatory response, its involvement in regulating the NLRP3 inflammasome in the context of allergic responses has not been extensively investigated to date. This study evaluated the expression patterns of the ANXA1 and NLRP3 proteins in human skin samples obtained from patients with atopic dermatitis (AD) and in mice with ovalbumin (OVA)-induced experimental AD. Furthermore, the in vitro effect of the ANXA1 mimetic peptide Ac2-26 on IL-4-stimulated human keratinocytes was evaluated.

Annexin A1 in neurological disorders: Neuroprotection and glial modulation.

Neurological disorders, such as neurodegenerative and neuroinflammatory diseases, have contributed significantly to global disability, even considering the rising life years expectations. Therefore, prevention, early diagnosis, and therapeutic alternatives have been essential to avoid the future collapse of health public systems. Annexin A1 (ANXA1), a Ca2 + -dependent protein, is a promising therapeutic candidate for neurological disorders.

Leaves Extracts Inhibit the Development of Ascitic and Solid Ehrlich Tumors.

is traditionally known for its medicinal properties. Objectives: Here, we investigated the effects of crude extract (CE) and ethyl acetate fraction (EAF) obtained from leaves on the ascitic (EA) and solid (ES) forms of Ehrlich tumors. : Induced and uninduced BALB/c mice were treated intramuscularly, for 7 or 14 days, with saline solution or CE and EAF, both at a 10% concentration, based on in vitro cytotoxicity assessment.

Expression patterns of Galectin-3 and NLRP3 in Chagas reactivation and graft damage in heart transplants.

Objective: This study aimed to assess the expression patterns of galectin-3 (Gal-3) and NLRP3 in heart transplant recipients according to the presence of reactivated Trypanosoma cruzi infection or allograft rejection in Chagas and non-Chagas heart transplant recipients.

Methods: Gal-3 and NLRP3 expression levels were analyzed in endomyocardial biopsies from 31 heart transplant recipients, including 16 patients with chronic Chagas disease (ChD) and 15 without ChD. Samples were evaluated during periods of graft rejection or ChD reactivation, characterized by intense myocardial cellular infiltrate, and after remission of the infiltrate, classified by histopathological severity.

Brief Disruption of Circadian Rhythms Alters Intestinal Barrier Integrity and Modulates DSS-Induced Colitis Severity in Mice.

Physiological processes in organisms exhibit circadian rhythms that optimize fitness and anticipate environmental changes. Luminal signals such as food or metabolites synchronize bowel activity, and disruptions in these rhythms are linked to metabolic disorders and gastrointestinal inflammation. To characterize the intrinsic intestinal rhythms and assess disruptions due to continuous darkness or light exposure, C57BL/6 mice were exposed to standard light-dark conditions or continuous light/darkness for 48 h, with evaluations at four timepoints.

Relationship between autophagy and NLRP3 inflammasome during articular cartilage degradation in oestrogen-deficient rats with streptozotocin-induced diabetes.

Background: Estrogen deficiency and Diabetes mellitus (DM) cause joint tissue deterioration, although the mechanisms are uncertain. This study evaluated the immunoexpression of autophagy and NLRP3-inflammasome markers, in rat articular cartilage with estrogen deficiency and DM.

Methods: Twenty rats were sham-operated (SHAM) or ovariectomized (OVX) and equally allocated into four groups: SHAM and OVX groups administered with vehicle solution; SHAM and OVX groups treated with 60 mg/kg/body weight of streptozotocin, intraperitoneally, to induce DM (SHAM-DM and OVX-DM groups).

Effect of modified citrus pectin on galectin-3 inhibition in cisplatin-induced cardiac and renal toxicity.

This study evaluated the effect of pharmacological inhibition of galectin 3 (Gal-3) with modified citrus pectin (MCP) on the heart and kidney in a model of cisplatin-induced acute toxicity. Male Wistar rats were divided into four groups (n = 6/group): SHAM, which received sterile saline intraperitoneally (i.p.

Lack of Annexin A1 Exacerbates Inflammatory Response in Acute Endometritis Model.

Annexin A1 (AnxA1) is a glucocorticoid-inducible protein and an important endogenous modulator of inflammation. However, its effect in the endometrial microenvironment is poorly explained. This study aimed to evaluate the role of endogenous AnxA1 in an endometritis mouse model induced by lipopolysaccharide (LPS).

Additional Insights Into the Role of Osteocalcin in Osteoblast Differentiation and in the Early Steps of Developing Alveolar Process of Rat Molars.

This study investigated whether osteocalcin (OCN) is present in osteoblast precursors and its relationship with initial phases of alveolar process formation. Samples of maxillae of 16-, 18-, and 20-day-old rat embryos (E16, E18, and E20, respectively), and 05-, 10-, and 15-day-old postnatal rats (P05, P10, and P15, respectively) were fixed and embedded in paraffin or araldite. Immunohistochemistry for osterix (Osx), alkaline phosphatase (ALP), and OCN detection was performed and the number of immunolabelled cells was computed.

Accumulation of sphingosine kinase 2 protein induces malignant transformation in oral keratinocytes associated with stemness, autophagy, senescence, and proliferation.

Sphingosine-1-phosphate (S1P) signaling has been widely explored as a therapeutic target in cancer. Sphingosine kinase 2 (SK2), one of the kinases that phosphorylate sphingosine, has a cell type and cell location-dependent mechanism of action, so the ability of SK2 to induce cell cycle arrest, apoptosis, proliferation, and survival is strongly influenced by the cell-context. In contrast to SK1, which is widely studied in different types of cancer, including head and neck cancer, the role of SK2 in the development and progression of oral cancer is still poorly understood.

Annexin A1 hydrogel improves healing properties in an experimental skin lesion after induction of type 1 diabetes.

Diabetes mellitus (DM) is characterized by metabolic alterations that involve defects in the secretion and/or action of insulin, being responsible for several complications, such as impaired healing. Studies from our research group have shown that annexin A1 protein (AnxA1) is involved in the regulation of inflammation and cell proliferation. In light of these findings, we have developed a new technology and evaluated its effect on a wound healing in vivo model using type 1 diabetes (T1DM)-induced mice.

Annexin A1, A2, A5, and A6 involvement in human pathologies.

The human genome codes for 12 annexins with highly homologous membrane-binding cores and unique amino termini, which endow each protein with its specific biological properties. Not unique to vertebrate biology, multiple annexin orthologs are present in almost all eukaryotes. Their ability to combine either dynamically or constitutively with membrane lipid bilayers is hypothetically the key property that has led to their retention and multiple adaptation in eukaryotic molecular cell biology.

Effects of inhibition of 5-lipoxygenase and 12-lipoxygenase pathways on skeletal muscle fiber regeneration.

We investigated the effect of inhibition of 5-lipoxigenase (LOX) and 12-LOX pathways on the regeneration of skeletal muscle fibers after injury induced by a myotoxin (MTX) phospholipase A from snake venom in an in vivo experimental model. Gastrocnemius muscles of mice injected with MTX presented an increase in 5-LOX protein expression, while 12-LOX was found to be a constitutive protein of skeletal muscle. Animals that received oral treatments with 5-LOX inhibitor MK886 or 12-LOX inhibitor baicalein 30 min and 48 h after MTX-induced muscle injury showed a reduction in the inflammatory process characterized by a significant decrease of cell influx and injured fibers in the degenerative phase (6 and 24 h after injury).

Bisphenol A disruption promotes mammary tumor microenvironment via phenotypic cell polarization and inflammatory response.

Inflammation in the established tumor microenvironment (TME) is often associated with a poor prognosis of breast cancer. Bisphenol A (BPA) is an endocrine-disrupting chemical that acts as inflammatory promoter and tumoral facilitator in mammary tissue. Previous studies demonstrated the onset of mammary carcinogenesis at aging when BPA exposure occurred in windows of development/susceptibility.

Deletion of Annexin A1 in Mice Upregulates the Expression of Its Receptor, Fpr2/3, and Reactivity to the AnxA1 Mimetic Peptide in Platelets.

Annexin A1 (ANXA1) is an endogenous protein, which plays a central function in the modulation of inflammation. While the functions of ANXA1 and its exogenous peptidomimetics, -Acetyl 2-26 ANXA1-derived peptide (ANXA1), in the modulation of immunological responses of neutrophils and monocytes have been investigated in detail, their effects on the modulation of platelet reactivity, haemostasis, thrombosis, and platelet-mediated inflammation remain largely unknown. Here, we demonstrate that the deletion of in mice upregulates the expression of its receptor, formyl peptide receptor 2/3 (, orthologue of human FPR2/ALX).