Nerve growth factor-mediated expression of galectin-3 in mouse dorsal root ganglion neurons

Pesheva, Penka; Kuklinski, Stephan; Biersack, Hans‐Jürgen; Probstmeier, Rainer

doi:10.1016/s0304-3940(00)01499-3

Cited by 26 publications

(18 citation statements)

References 15 publications

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“…Recently dorsal root ganglia neurons have been identified as dependent on Runx3 in their development (48). Dorsal root ganglia cells also express significant amounts of galectin-3 (50). Therefore, it is tempting to speculate that Runt factors control galectin-3 expression at these extraskeletal sites.…”

Section: Discussionmentioning

confidence: 99%

Expression of Galectin-3 in Skeletal Tissues Is Controlled by Runx2

Stöck

Schäfer

Stricker

et al. 2003

Journal of Biological Chemistry

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The ␤-galatoside-specific lectin galectin-3 is expressed in vivo in osteoblasts as well as in epiphyseal cartilage. Here we show that in vitro, galectin-3 expression is upregulated in the preosteoblastic cell line MC3T3-E1 during the matrix maturation stage of the osteoblast developmental sequence. Expression persists into late differentiation stages when the mature osteoblastic phenotype is established. The skeletal expression pattern of galectin-3 overlaps at many sites with that of the transcription factor Runx2. Runx2 is a key regulator of osteoblast development and necessary for chondrocyte differentiation in the growth plate. Both human and mouse galectin-3 promoters contain putative Runxbinding sites. The constitutive or inducible forced expression of Runx2 is sufficient for the onset of galectin-3 transcription in the mesenchymal precursor cell line C3H10T1/2. Moreover, Runx2 is able to bind to at least two sites in the galectin-3 promoter region. The crucial role of Runx2 was confirmed in Runx2-deficient mice, which are devoid of galectin-3 expression in skeletal cells. The overlapping expression pattern of galectin-3 with the other two members of the Runt family of transcription factors (Runx1 and Runx3) points to a potential regulation of the galectin-3 gene (LGALS3) by these factors in hematopoietic, skin, and dorsal root ganglial cells.

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Section: Discussionmentioning

confidence: 99%

Expression of Galectin-3 in Skeletal Tissues Is Controlled by Runx2

Stöck

Schäfer

Stricker

et al. 2003

Journal of Biological Chemistry

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“…GAL-3 is expressed in a variety of cells, e.g., endothelial and epithelial cells, activated macrophages, microglial cells, basophils, mast cells, neutrophils, neurons and cardiomyocytes [10][11][12][13][14][15][16]. So far we know that GAL-3 is closely associated with myocardial infarction in the early post MI period and later with myocardial fibrosis and heart failure [15,17].…”

Section: Introductionmentioning

confidence: 99%

Myocardial Ischemia Reperfusion Injury: Apoptotic, Inflammatory and Oxidative Stress Role of Galectin-3

Al-Salam

Hashmi

2018

Cell Physiol Biochem

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Background/Aims: Myocardial reperfusion has the potential to salvage the ischemic myocardium after a period of coronary occlusion. Reperfusion, however, can cause a wide spectrum of deleterious effects. Galectin-3 (GAL-3), a beta galactoside binding lectin, is closely associated with myocardial infarction (MI), myocardial fibrosis and heart failure. In our study, we investigated its role in ischemia-reperfusion injuries (IR) as this phenomenon is extremely relevant to the early intervention after acute MI. Methods: C57B6/J wild type (WT) mice and GAL-3 knockout (KO) mice were used for murine model of IR injury in the heart where a period of 30 minutes ischemia was followed by 24 hours of reperfusion. Heart samples were processed for immunohistochemical and immunofluorescent labeling, morphometric analysis, western blot and enzyme-linked immunosorbent assay to identify the apoptotic, inflammatory and oxidative stress role of GAL-3. Results: Our results show that there was a significant increase in GAL-3 levels in the heart which shows GAL-3 is playing a role in the ischemia reperfusion injury. Troponin I was also significantly higher in GAL-3-KO group than wild type. Our study shows that GAL-3 is associated with an increase in the antioxidant activity in the IR injured myocardium. Antioxidant enzymes superoxide dismutase, glutathione and catalase were found to be significantly raised in the GAL-3 wild type IR as compared to the GAL-3 KO IR group. A significant increase in apoptotic activity is seen in GAL-3 KO IR group as compared with GAL-3 wild IR group. Conclusion: Our study shows that GAL-3 can affect the redox pathways, controlling cell survival and death, and plays a protective role on the myocardium following IR injury.

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“…GAL-3 is expressed in a variety of cells, e.g., endothelial and epithelial cells; activated macrophages [39][40][41]; activated microglial cells [42,43]; inflammatory cells including macrophages, basophils, mast cells, eosinophils, and neutrophils [44][45][46][47][48]; and subsets of neurons [49]. In tissues, GAL-3 is expressed in the lung, spleen, stomach, colon, adrenal gland, uterus, ovary, prostate, kidney, heart, cerebrum, pancreas, and liver [50].…”

Section: Introductionmentioning

confidence: 99%