The effects of galectin‐3 depletion apheresis on induced skin inflammation in a porcine model

Navarro-Alvarez, Nalú; Gonçalves, Beatriz M; Andrews, Alec R.; Wang, Zhaohui; Harrington, Edward; Shah, Jigesh A.; Sachs, David H.; Eliaz, Isaac; Huang, Christene A.

doi:10.1002/jca.21624

Cited by 6 publications

(6 citation statements)

References 30 publications

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“…However, a double-blind evaluation of plasmapheresis in ten patients with schizophrenia yielded negative results, and the procedure did not lead to a reduction in psychosis[ 72 ]. As hypercholesterolemia has been treated with plasmapheresis, and recently the therapeutic usefulness of Gal-3 depletion apheresis has been demonstrated in inflammation-mediated disease, targeting Gal-3 molecule may be a useful way to address immunometabolic problems and cognitive deterioration in schizophrenia in the future[ 73 , 74 ].…”

Section: Discussionmentioning

confidence: 99%

Galectin-3 possible involvement in antipsychotic-induced metabolic changes of schizophrenia: A minireview

Borovcanin¹,

Vesić²,

Jovanović³

et al. 2021

WJD

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Recently, specific immunometabolic profiles have been postulated in patients with schizophrenia, even before full-blown disease and independent of antipsychotic treatment. Proteomic profiling studies offer a promising potential for elucidating the cellular and molecular pathways that may be involved in the onset and progression of schizophrenia symptoms, and co-occurrent metabolic changes. In view of all this, we were intrigued to explore galectin-3 (Gal-3) as a glycan, and in our previous study, we measured its elevated levels in remission of schizophrenia. The finding may be a consequence of antipsychotic treatment and may have an impact on the onset of inflammation, the development of obesity, and the presumed cognitive changes in schizophrenia. In the animal study, it was shown that downregulation of Gal-3 was beneficial in insulin regulation of obesity and cognitive preservation. Strategies involving plasma exchange are discussed in this review, particularly in the context of Gal-3 elimination.

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Section: Discussionmentioning

confidence: 99%

Galectin-3 possible involvement in antipsychotic-induced metabolic changes of schizophrenia: A minireview

Borovcanin¹,

Vesić²,

Jovanović³

et al. 2021

WJD

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“…However, selectively removing Gal-3 through therapeutic apheresis may serve as a potential therapeutic approach. In a porcine model of in ammatory skin induration, Gal-3-speci c therapeutic apheresis resulted in a signi cant, rapid decrease in skin in ammation, as well as faster resolution of skin injury [55]. Apheresis can remove Gal-3 rapidly and e ciently, and can be repeated as needed.…”

Section: Discussionmentioning

confidence: 99%

Galectin-3 In Septic Acute Kidney Injury: A Translational Study

Sun

Jiang

Eliaz

et al. 2021

Preprint

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Background Galectin-3 (Gal-3) is a pleiotropic glycan-binding protein shown to be involved in sepsis and acute kidney injury (AKI). However, its role has never been elucidated in sepsis-associated AKI (S-AKI). We aimed to explore Gal-3’s role and its potential utility as a therapeutic target in S-AKI. MethodsIn 57 patients admitted to the intensive care unit (ICU) with sepsis, serum Gal-3 was examined as a predictor of ICU mortality and AKI. In a rat model of S-AKI induced by cecal ligation and puncture (CLP), 7-day mortality and serum Gal-3, IL-6, and creatinine were examined at baseline, 2, 8, and 24 hours (h) post-CLP. Two experimental groups received the Gal-3 inhibitor modified citrus pectin (P-MCP) at 400 mg/kg/day and 1200 mg/kg/day, while the control group received water only (n = 18 in each group). ResultsAmong 57 patients, 27 developed AKI and 8 died in the ICU. Serum Gal-3 was an independent predictor of AKI (OR = 1.2 [95% CI 1.1-1.4], p = 0.01) and ICU mortality (OR = 1.4 [95% CI 1.1-2.2], p = 0.04) before and after controlling for age, AKI, and acute physiology and chronic health evaluation (APACHE II) score. In the CLP rat experiment, serum Gal-3 peaked earlier than Interleukin-6 (IL-6). Serum Gal-3 was significantly lower in both P-MCP-treated groups compared to control at 2 h post-CLP (400 mg: p = 0.003; 1200 mg: p = 0.002), and IL-6 was significantly lower in both P-MCP-treated groups at all time points with a maximum difference at 24 h post-CLP (400 mg: p = 0.015; 1200 mg: p = 0.02). In the Gal-3 inhibitor groups, 7-day mortality was significantly reduced from 61% in the control group to 28% (400 mg P-MCP: p = 0.03) and 22% (1200 mg P-MCP: p = 0.001). Rates of AKI per RIFLE criteria were significantly reduced from 89% in the control group to 44% in both P-MCP-treated groups (400mg: p = 0.007; 1200mg: p = 0.007). ConclusionsThis translational study demonstrates the importance of Gal-3 in the pathogenesis of S-AKI, and its potential utility as a therapeutic target.

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“…However, the mechanistic role of galectin-3 in cGVHD models has not been investigated, so whether galectin-3 is implicated in the causal pathway of cGVHD pathophysiology or serves a secondary marker of inflammation is unknown. This is of particular interest, as animal models have demonstrated that galectin-3 function can be reduced by exposure to modified citrus pectin [ 15 , 16 ], and that galectin-3 can be depleted through therapeutic apheresis [ 17 ], suggesting that galectin-3 could be a potential target for therapeutic intervention.…”

Section: Discussionmentioning

confidence: 99%

Elevated Galectin-3 Plasma Concentrations in Recipients of Allogeneic Hematopoietic Cell Transplantation

DeFilipp¹,

Navarro-Alvarez²,

Li³

et al. 2019

CHI

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Galectin-3 is a beta-galactoside-binding lectin with an established association to inflammatory and fibrotic conditions. We investigated galectin-3 levels in 68 recipients of allogeneic hematopoietic cell transplantation (HCT) to look for associations with chronic graft-versus-host disease (cGVHD). Plasma galectin-3 concentrations were measured at 1 year post-HCT and correlated with clinical data collected from individual medical records. The median serum galectin-3 level at that time point was 14.9 ng/mL (range, 5.5-61.6), which was significantly higher than that among healthy controls (14.9 versus 6.2, p < 0.001). Furthermore, patients with active cGVHD at the time of sample collection had higher median levels as compared to those without cGVHD (16.9 versus 13, p = 0.03). In a multivariable logistic model, there was no significant association between the presence of cGVHD at the date of sample collection and elevated galectin-3 levels (>14.9 ng/mL) (odds ratio [OR]: 2.03 (0.60, 6.88), p = 0.26). However, among patients with cGVHD at the date of sample collection, active systemic corticosteroid therapy was associated with elevated galectin-3 levels (OR: 20.32 (1.66, 249.39), p = 0.02). Furthermore, in a competing risk regression model, elevated galectin-3 levels at 1 year post-HCT were not associated with future development of moderate or severe cGVHD (OR: 1.24 (0.21, 7.45), p = 0.81). In conclusion, plasma galectin-3 concentrations are elevated in recipients of allo-HCT, especially among patients with cGVHD. Further investigation will be required to determine whether galectin-3 has a pathophysiologic role in cGVHD or serves as a marker of ongoing inflammation following allogeneic HCT.

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The effects of galectin‐3 depletion apheresis on induced skin inflammation in a porcine model

Cited by 6 publications

References 30 publications

Galectin-3 possible involvement in antipsychotic-induced metabolic changes of schizophrenia: A minireview

Galectin-3 possible involvement in antipsychotic-induced metabolic changes of schizophrenia: A minireview

Galectin-3 In Septic Acute Kidney Injury: A Translational Study

Elevated Galectin-3 Plasma Concentrations in Recipients of Allogeneic Hematopoietic Cell Transplantation

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