Cytoplasmic Shedding as a Mode of Formation of Lymphocyte-Like Blast Cells by Newt Histiocytes

Rondanelli, E. G.; Magliulo, E; Carosi, Giampiero; Dionisi, Davide

doi:10.1159/000208887

Cited by 4 publications

(3 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Autophagy can be inhibited by chloroquine (CQ) as it accumulates within autophagosomes, and inhibits the fusion with lysosomes thereby preventing the formation of autolysosomes. This reduction by chloroquine in the final phase of autophagy that provides a pathway for the breakdown of proteins and removal of metabolic debris from the cell, may augment apoptosis [66-68] or rescue osteocyte from cell death [69]. Recently Xia et al reported that dexamethasone treatment of an osteocytic cell line, MLO-Y4 cells, increased autophagy markers and the accumulation of autophagosome vacuoles as detected by several standard approaches based on recently published guidelines including fluorescent GFP-LC3 punctate dots, MDC fluorescence, LC3 lipidation and electron microscopy imaging in addition to conventional acridine orange staining [70].…”

Section: Does Autophagy Explain the Osteocyte Response To Gcs?mentioning

confidence: 99%

Glucocorticoids and osteocyte autophagy

Yao

Dai

Jiang

et al. 2013

Bone

View full text Add to dashboard Cite

Glucocorticoids are used for the treatment of inflammatory and autoimmune diseases. While they are effective therapy, bone loss and incident fracture risk is high. While previous studies have found GC effects on both osteoclasts and oteoblasts, our work has focused on the effects of GCs on osteocytes. Osteocytes exposed to low dose GCs undergo autophagy while osteocytes exposed to high doses of GCs or for a prolonged period of time undergo apoptosis. This paper will review the data to support the role of GCs in osteocyte autophagy.

show abstract

Section: Does Autophagy Explain the Osteocyte Response To Gcs?mentioning

confidence: 99%

Glucocorticoids and osteocyte autophagy

Yao

Dai

Jiang

et al. 2013

Bone

View full text Add to dashboard Cite

show abstract

“…To our knowledge, the only other incidence of cytoplasmic shedding of leukocytes known among vertebrates is that which was reported to occur in newt histiocytes, which supposedly engage in this activity as a mode of forming lymphoid cells (Rondanelli et al. ). We have no explanation other than to suggest that the leukocyte cytoplasmic shedding observed here may possibly be a case of functional adaptation induced by entry of these cells into the testicular microenvironment, possibly necessitated by the need for the leukocyte to traverse the connective tissue‐rich RZ to carry out non‐phagocytic actions.…”

Section: Discussionmentioning

confidence: 99%

The epigonal organ and mature pole of the testis in the recreationally fished blue shark (Prionace glauca): histochemico‐functional correlates

McClusky

Sulikowski

2014

Journal of Anatomy

View full text Add to dashboard Cite

The exact role of the immune system in normal spermatogenesis is poorly understood. The attachment, however, of the lymphomyeloid epigonal organ specifically to the testis's mature pole in many shark species is a curious finding. Unlike the histology of the lymphomyeloid tissues of many other elasmobranchs, the epigonal organ leukocytes of wild-caught blue shark (Prionace glauca), besides exhibiting extensive nuclear heterogeneity, contain some of the largest known granules ever seen in vertebrate white blood cells. It was previously shown that the blue shark epigonal organ remains unremarkable and functionally unchanged despite cestode parasites embedded into its surface, suggesting that it might have other functions in addition to microbial defense. We show here that Prionace epigonal leukocytes shed their granule-laden cytoplasm into the cyst resorption zone (RZ) of the testis, i.e. the region separating the spermatogenic tissue from the epigonal organ, as they begin to migrate into the RZ. Using the immunoreactivity of the conserved transcription factor (proliferating cell nuclear antigen) as marker, it is shown that the granule-lacking leukocytes exclusively infiltrated spermatozoal cysts leftover after the wave of wide-spread multinuclear cell death in summer-breeding males in a seasonally dependent manner. By contrast, Prionace caught 2 months later showed fully recovered testes containing numerous completely intact spermatozoal cysts. Conversely, degenerating immature spermatids were gradually phagocytized by their accompanying Sertoli cells, and leukocytes did not infiltrate such cysts. The autoimmune response described here resembles in every aspect the testicular autoimmune response induced experimentally in a teleost fish. These observations suggest functional adaptation of shark leukocytes in response to specific changes in the testicular microenvironment.

show abstract

“…Autophagy can be inhibited by chloroquine (CQ) as it accumulates within autophagosomes and then inhibits fusion with lysosomes, thereby preventing the formation of autolysosomes. This reduction by chloroquine in the final phase of autophagy, which provides a pathway for the breakdown of proteins and removal of metabolic debris from the cell, may augment apoptosis (53-55) or rescue osteocytes from cell death (56).…”

Section: Osteocyte Autophagy Induced By Gcsmentioning

confidence: 99%

New insights into the biology of glucocorticoid-induced osteoporosis

Lane¹,

Yao²

2011

IBMS BoneKEy

View full text Add to dashboard Cite

Glucocorticoid (GC) use results in rapid bone loss and elevated fracture risk. The excess bone fragility from GC treatment is multi-factorial. GCs alter calcium and phosphorus metabolism, which can result in elevation of parathyroid hormone (PTH) and early stimulation of osteoclast activity and bone remodeling, followed by a delayed but sustained reduction in osteogenesis, osteoblast activity and osteocyte metabolism. The changes in bone cell viability with GCs results in reduction of localized and whole bone strength. New data reveal that GC use may influence mineral metabolism through FGF23. The altered perilacunar mineralization around GC-treated osteocytes may be secondary to increased FGF23 production. In addition, low doses of GCs can induce self-preservation of osteocytes through the molecular mechanisms of autophagy, while higher doses of GCs induce osteocyte apoptosis. Osteocytic autophagy may allow for cell survival and then, with withdrawal of GCs, for the repair of lost bone tissue. Currently, both antiresorptive and anabolic agents are prescribed to prevent or treat GC-induced bone loss. Additional studies are needed to further explore whether current treatments used for GC-induced bone loss alter osteocyte metabolism and how this influences localized and whole bone strength. IBMS BoneKEy. 2011 May;8(5):229-236.

show abstract

Cytoplasmic Shedding as a Mode of Formation of Lymphocyte-Like Blast Cells by Newt Histiocytes

Cited by 4 publications

References 10 publications

Glucocorticoids and osteocyte autophagy

Glucocorticoids and osteocyte autophagy

The epigonal organ and mature pole of the testis in the recreationally fished blue shark (Prionace glauca): histochemico‐functional correlates

New insights into the biology of glucocorticoid-induced osteoporosis

Contact Info

Product

Resources

About