STAT-6 mediates TRAIL induced RANK ligand expression in stromal/preosteoblast cells

Sundaram, Kumaran; Sambandam, Yuvaraj; Balasubramanian, Sundaravadivel; Pillai, Balakrishnan; Voelkel‐Johnson, Christina; Ries, William L.; Reddy, Sakamuri V.

doi:10.1016/j.bone.2014.10.016

Cited by 14 publications

(12 citation statements)

References 54 publications

(61 reference statements)

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“…Ablation study in tendon demonstrated that M1 promoted inflammation and repair process during early stage, whereas M2 suppress inflammation and resolving scarring at later stage (Millar et al, ). Meanwhile, diverse signal pathways were activated at different stages of tendinopathy to express certain genes and proteins (Sundaram et al, ). Based on the transition in inflammation activation signatures, diverse therapeutic interventions at different disease stages may be applicable (Dakin et al, ; Thomopoulos et al, ).…”

Section: Discussionmentioning

confidence: 99%

Intratendon delivery of leukocyte‐rich platelet‐rich plasma at early stage promotes tendon repair in a rabbit Achilles tendinopathy model

Jiang

et al. 2020

J Tissue Eng Regen Med

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Tendinopathy is a great obstacle in clinical practice due to its poor regenerative capacity. The influence of different stages of tendinopathy on effects of leukocyte‐rich platelet‐rich plasma (Lr‐PRP) has not been elucidated. The aim of this study is to investigate the optimal time point for delivery of Lr‐PRP on tendinopathy. A tendinopathy model was established by local collagenase injection on the rabbit Achilles tendon. Then after collagenase induction, following treatments were applied randomly on the lesion: (a) 200 μl of Lr‐PRP at 1 week (PRP‐1 group), (b) 200 μl of saline at 1 week (Saline‐1 group), (c) 200 μl of Lr‐PRP at 4 weeks (PRP‐2 group), and (d) 200 μl of saline at 4 weeks (Saline‐2 group). Six weeks after collagenase induction, outcomes were assessed by magnetic resonance imaging, cytokine quantification, gene expression, histology, and transmission electron microscopy. Our results demonstrated that PRP‐1 group had the least cross‐sectional area and lesion percent of the involved tendon, as well as the lowest signal intensity in magnetic resonance imaging among all groups. However, the PRP‐2 group showed larger cross‐sectional area than saline groups. Enzyme‐linked immunosorbent assay indicated that PRP‐1 group had a higher level of interleukin‐10 but lower level of interleukin‐6 when compared with PRP‐2 and saline groups. Meanwhile, the highest expression of collagen (Col) 1 in PRP‐1 and Col 3, matrix metalloproteinase (MMP)‐1, and MMP‐3 in PRP‐2 was found. Histologically, the PRP‐1 showed better general scores than PRP‐2, and no significant difference was found between the PRP‐2 and saline groups. For transmission electron microscopy, PRP‐1 had the largest mean collagen fibril diameter, and the PRP‐2 group showed even smaller mean collagen fibril diameter than saline groups. In conclusion, intratendon delivery of Lr‐PRP at early stage showed beneficial effect for repair of tendinopathy but not at late stage. For translation of our results to clinical circumstances, further studies are still needed.

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Section: Discussionmentioning

confidence: 99%

Intratendon delivery of leukocyte‐rich platelet‐rich plasma at early stage promotes tendon repair in a rabbit Achilles tendinopathy model

Jiang

et al. 2020

J Tissue Eng Regen Med

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“…Moreover, this group also reported increased bone mass in mice treated with recombinant TRAIL [187] but this could not be confirmed by Labrinidis et al [188]. It has been recently found that TRAIL upregulates RANKL expression in the preosteoblast cell line SAKA-T [189]. Thus, at least TRAIL may exert in vivo also indirect RANKL-mediated osteoclastic activity not evident from the above-cited in vitro studies that may superimpose with its direct effects on preosteoclasts/osteoclasts.…”

Section: Cd95l-and Trail-induced Cellular Differentiationmentioning

confidence: 94%

“…. It has been recently found that TRAIL upregulates RANKL expression in the preosteoblast cell line SAKA‐T . Thus, at least TRAIL may exert in vivo also indirect RANKL‐mediated osteoclastic activity not evident from the above‐cited in vitro studies that may superimpose with its direct effects on preosteoclasts/osteoclasts.…”

Section: Cd95l‐ and Trail‐induced Cellular Differentiationmentioning

confidence: 99%

Cell death‐independent activities of the death receptors CD95, TRAILR1, and TRAILR2

2016

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Since their identification more than 20 years ago, the death receptors CD95, TRAILR1, and TRAILR2 have been intensively studied with respect to their cell death-inducing activities. These receptors, however, can also trigger a variety of cell death-independent cellular responses reaching from the activation of proinflammatory gene transcription programs over the stimulation of proliferation and differentiation to induction of cell migration. The cell death-inducing signaling mechanisms of CD95 and the TRAIL death receptors are well understood. In contrast, despite the increasing recognition of the biological and pathophysiological relevance of the cell death-independent activities of CD95, TRAILR1, and TRAILR2, the corresponding signaling mechanisms are less understood and give no fully coherent picture. This review is focused on the cell death-independent activities of CD95 and the TRAIL death receptors and addresses mainly three questions: (a) how are these receptors linked to noncell death pathways at the molecular level, (b) which factors determine the balance of cell death and cell death-independent activities of CD95 and the TRAIL death receptors at the cellular level, and (c) what are the consequences of the cell death-independent functions of these receptors for their role in cancer and inflammatory diseases.

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“…Mother-offspring group studies have shown that maternal vitamin D insufficiency leads to reduced bone mass during childhood 35, 36 . We recently demonstrated that TRAIL enhances bone-resorbing osteoclast differentiation 37, 38 . Therefore, elevated levels of TRAIL expression due to vitamin D deficiency may have a significant impact on both mother and infant bone growth/development.…”

Section: Discussionmentioning

confidence: 99%

Vitamin D Modulation of TRAIL Expression in Human Milk and Mammary Epithelial Cells

Sambandam

Reddy

Mulligan

et al. 2017

Sci Rep

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The vitamin D levels in mothers affect the health status of both the mother and breastfeeding infant. Vitamin D deficient mothers’ infants are prone to rickets. While tumor necrosis factor-related apoptosis inducing ligand (TRAIL) has been implicated in cellular growth/apoptosis, immune cell function and bone-resorbing osteoclast formation, the expression of TRAIL in human milk as a function of vitamin D status in mothers remains unknown. We hypothesized that vitamin D deficiency alters TRAIL protein levels in human breast milk and mammary epithelial cells. Milk from vitamin D deficient mothers showed high levels of TRAIL (α and β) proteins compared to milk from vitamin D replete women. Western blot analysis of total cell lysate obtained from normal human mammary epithelial (HME-1) cells treated with variable doses (0–20 nM) of vitamin D for 24 h demonstrated that low levels (0.5 to 5 nM) significantly increased the TRAIL α but no change in β expression. In contrast, vitamin D at 20 nM concentration suppressed the expression of both TRAIL α and β proteins. Consistently, vitamin D regulated TRAIL mRNA expression in HME-1 cells. Our results indicate that vitamin D status in mothers modulates TRAIL expression in breast milk, which may have implications for both mother and infant health.

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STAT-6 mediates TRAIL induced RANK ligand expression in stromal/preosteoblast cells

Cited by 14 publications

References 54 publications

Intratendon delivery of leukocyte‐rich platelet‐rich plasma at early stage promotes tendon repair in a rabbit Achilles tendinopathy model

Intratendon delivery of leukocyte‐rich platelet‐rich plasma at early stage promotes tendon repair in a rabbit Achilles tendinopathy model

Cell death‐independent activities of the death receptors CD95, TRAILR1, and TRAILR2

Vitamin D Modulation of TRAIL Expression in Human Milk and Mammary Epithelial Cells

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