Sulf1 and Sulf2 expression in the nervous system and its role in limiting neurite outgrowth in vitro

Joy, Mary; Vrbová, Gerta; Dhoot, Gurtej K.; Anderson, Patrick N.

doi:10.1016/j.expneurol.2014.10.011

Cited by 20 publications

(20 citation statements)

References 55 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our studies show that cartilage and bone cells do not follow this trend but instead retain an easily detectable level of both SULF1 and SULF2 expression in postnatal and adult skeletal elements that also agrees with previous studies demonstrating some Sulf1/Sulf2 expression in fetal and postnatal tissues (Zhao et al 2006;Otsuki et al 2008;Ratzka et al 2008). Previously, only adult neuronal tissues have been found to express high levels of these enzymes (Joy et al 2015); some low level expression in endothelial cells has been documented where they have been shown to act as cell signalling inhibitors (Sahota and Dhoot 2009). Continued expression of SULF1/SULF2 by chondrocytes in postnatal cartilage may also relate to some inhibitory role although SULF expression was not observed in all chondrocytes.…”

Section: Discussionsupporting

confidence: 93%

“…The detection of some SULF-positive and SULFnegative articular chondrocytes, however, indicates the varying levels of chondrocytic activity or quiescence. In neuronal tissue, SULFs persist in the adult to inhibit cell proliferation and neurite outgrowth (Joy et al 2015). It is not clear if the expression and non-detection of SULFs in a subset of cells represents activity versus quiescence since the chondrocytes are not known to undergo significant cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Expression of Sulf1 and Sulf2 in cartilage, bone and endochondral fracture healing

Zaman

Staines

Farquharson

et al. 2015

Histochem Cell Biol

View full text Add to dashboard Cite

Highlights: High Sulf1/Sulf2 expression in active osteoblasts with reduction in osteocytes. High variability in Sulf1/Sulf2 expression in articular chondrocytes. Hypertrophic chondrocytes in growing and healing bone express high levels of Sulf2 but not Sulf1. High Sulf2 expression in growing and healing bone closely correlates with Hedgehog signalling.ABSTRACT: SULF1/SULF2 enzymes regulate cell signalling that impacts the growth and differentiation of many tissues. To determine their possible role in cartilage and bone growth or repair, their expression was examined during development and bone fracture healing using RT-PCR and immunochemical analyses. Examination of epiphyseal growth plates revealed differential, inverse patterns of SULF1 and SULF2 expression, with the former enriched in quiescent and the latter in hypertrophic chondrocyte zones. Markedly higher levels of both SULFs, however, were expressed in osteoblasts actively forming bone when compared with proliferating pre-osteoblasts in the periosteum or the entombed osteocytes which express the lowest levels. The increased Sulf1 and Sulf2 expression in differentiating osteoblasts was further confirmed by RT PCR analysis of mRNA levels in rat calvarial osteoblast cultures.SULF1 and SULF2 were expressed in most fetal articular chondrocytes but downregulated in a larger subset of cells in the postnatal articular cartilage. Unlike adult articular chondrocytes, SULF1/SULF2 expression varied markedly in postnatal hypertrophic chondrocytes in the growth plate, with very high SULF2 expression compared with SULF1 apparent during neonatal growth in both primary and secondary centres of ossification. Similarly, hypertrophic chondrocytes expressed greatly higher levels of SULF2 but not SULF1 during bone fracture healing. SULF2 expression unlike SULF1 also spread to the calcifying matrix around the hypertrophic chondrocytes indicating its possible ligand inhibiting role through HSPG desulfation. Higher levels of SULF2 in both developing and healing bone closely correlated with parallel increases in hedgehog signalling analysed by ptc1 receptor expression.

show abstract

Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Expression of Sulf1 and Sulf2 in cartilage, bone and endochondral fracture healing

Zaman

Staines

Farquharson

et al. 2015

Histochem Cell Biol

View full text Add to dashboard Cite

show abstract

“…This is compatible with increased expression of Sulfs during fetal development of many tissues (Gill et al 2010;Hitchins et al 2013) and during the development of different tumour types (Gill et al 2012;Gill et al 2014;Lemjabbar-Alaoui et al). It, however, differs from some other studies reporting Sulf1 to be a tumour suppressor in liver (Lai et al 2006;Lai et al 2008a;Xu G et al 2014) thus implying higher level of expression in normal adult liver although some other adult tissues such as neuronal and skeletal tissues have been reported to continue expressing Sulf1/Sulf2 throughout life (Joy et al 2015;Zaman et al 2016). Sulf1 activation, however is not unique to fetal or tumour growth since a number of other conditions including injury-induced repair can also activate these enzymes.…”

Section: Discussionsupporting

confidence: 61%

SULF1/SULF2 reactivation during liver damage and tumour growth

Graham

Murphy

Dhoot

2016

Histochem Cell Biol

Self Cite

View full text Add to dashboard Cite

“…Changes in Sulf1 and Sulf2 expression modulate sulfation of glial cell HS and regulate FGF1 and FGF9 signaling in glial cells and control nervous system repair in rats [27] and mice [28]. While Sulf1 and Sulf2 are expressed in many different types of neurons in the nervous system, there are differences in their regional distribution, subcellular localization, and glycosylation in different parts of the nervous system [29]. …”

Section: Introductionmentioning

confidence: 99%

Decreased Expression of Sulfatase 2 in the Brains of Alzheimer’s Disease Patients: Implications for Regulation of Neuronal Cell Signaling

Roberts

Kang

et al. 2017

ADR

View full text Add to dashboard Cite

Background The human sulfatase 1 (SULF1) and sulfatase 2 (SULF2) genes modulate cell signaling and homeostasis in many tissues. Gene expression analyses have implicated SULF2 in disease pathogenesis, including Alzheimer’s disease (AD), but changes in brain SULF2 expression have not been directly established. Objective To investigate the expression of SULF1 and SULF2 in brain tissues from AD cases and cognitively normal controls. Methods Autopsy tissue from AD cases (n = 20) and age-and gender-matched cognitively normal controls (n = 20) were identified from the Mayo Clinic Alzheimer’s Disease Patient Registry neuropathology database. Tissue slides were stained for SULF1 and SULF2 protein expression in the hippocampus and frontal lobe and an expression score computed from the proportion of cells stained and the intensity of staining (range 0 [no expression] to 9 [marked expression]). Results SULF2 expression was reduced in AD cases. Compared to cognitively normal controls, SULF2 expression in AD cases was significantly decreased in the hippocampal Cornu Ammonis (CA) (mean score of 6.5 in cases versus 8.3 in controls; p = 0.003), in the gray matter of the parahippocampal gyrus (5.6 in cases versus 7.6 in controls; p = 0.003), and in the frontal lobe gray matter (5.4 in cases versus 7.4 in controls; p = 0.002). There was no difference in SULF1 expression in the hippocampus or frontal lobe of AD cases and controls. As expected there were no differences in SULF1 or SULF2 expression in white matter in AD cases compared to cognitively normal controls. Conclusion Decresed SULF2 in specific regions of the brain occurs in AD.

show abstract

Sulf1 and Sulf2 expression in the nervous system and its role in limiting neurite outgrowth in vitro

Cited by 20 publications

References 55 publications

Expression of Sulf1 and Sulf2 in cartilage, bone and endochondral fracture healing

Expression of Sulf1 and Sulf2 in cartilage, bone and endochondral fracture healing

SULF1/SULF2 reactivation during liver damage and tumour growth

Decreased Expression of Sulfatase 2 in the Brains of Alzheimer’s Disease Patients: Implications for Regulation of Neuronal Cell Signaling

Contact Info

Product

Resources

About