Vastly extended drug release from poly(pro-17β-estradiol) materials facilitates in vitro neurotrophism and neuroprotection

D’Amato, Anthony R.; Puhl, Devan L; Ellman, Samuel A. T.; Balouch, Bailey; Gilbert, Ryan J.; Palermo, Edmund F.

doi:10.1038/s41467-019-12835-w

Cited by 22 publications

(25 citation statements)

References 65 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Neurite outgrowth from whole DRG explants was determined using images of whole DRG cultured on each fiber type and stained for neurofilament to investigate whether fingolimod released from electrospun fibers enhances neurite extension. Using FIJI software, the lengths of the five longest neurites on each side of the DRG body were measured by drawing a line from the edge of the DRG body to the tip of each neurite ( D’Amato et al, 2019a ). The measurements were recorded and the average neurite length per side was calculated.…”

Section: Methodsmentioning

confidence: 99%

Aligned Fingolimod-Releasing Electrospun Fibers Increase Dorsal Root Ganglia Neurite Extension and Decrease Schwann Cell Expression of Promyelinating Factors

Puhl

Funnell

D’Amato

et al. 2020

Front. Bioeng. Biotechnol.

Self Cite

View full text Add to dashboard Cite

Fingolimod-Releasing Biomaterial Fibers fingolimod-loaded fibers enhanced neurite outgrowth from whole and dissociated DRG neurons, increased Schwann cell migration, and reduced the Schwann cell expression of promyelinating factors. The in vitro findings show the potential of the aligned fingolimod-releasing electrospun fibers to enhance peripheral nerve regeneration and serve as a basis for future in vivo studies.

show abstract

Section: Methodsmentioning

confidence: 99%

Aligned Fingolimod-Releasing Electrospun Fibers Increase Dorsal Root Ganglia Neurite Extension and Decrease Schwann Cell Expression of Promyelinating Factors

Puhl

Funnell

D’Amato

et al. 2020

Front. Bioeng. Biotechnol.

Self Cite

View full text Add to dashboard Cite

show abstract

“…This protection has been related to the action of 17 β -estradiol promoting neurite extension ex vivo and protecting neurons from oxidative stress in vitro. Here, we have found an estradiol-like molecule, the 4-hydroxy-17beta-estradiol-2-S-glutathione that can act in this mechanism [ 46 ].…”

Section: Discussionmentioning

confidence: 99%

Box Jellyfish (Cnidaria, Cubozoa) Extract Increases Neuron’s Connection: A Possible Neuroprotector Effect

Arruda

Vigerelli

Búfalo

et al. 2021

BioMed Research International

View full text Add to dashboard Cite

Neurodegenerative diseases are one of the major causes of death worldwide, characterized by neurite atrophy, neuron apoptosis, and synapse loss. No effective treatment has been indicated for such diseases so far, and the search for new drugs is being increased in the last years. Animal venoms’ secretion/venom can be an alternative for the discovery of new molecules, which could be the prototype for a new treatment. Here, we present the biochemical characterization and activity of the extract from the box jellyfish Chiropsalmus quadrumanus (Cq) on neurites. The Cq methanolic extract was obtained and incubated to human SH-SY5Y neurons, and neurite parameters were evaluated. The extract was tested in other cell types to check its cytotoxicity and was submitted to biochemical analysis by mass spectrometry in order to check its composition. We could verify that the Cq extract increased neurite outgrowth length and branching junctions, amplifying the contact between SH-SY5Y neurons, without affecting cell body and viability. The extract action was selective for neurons, as it did not cause any effects on other cell types, such as tumor line, nontumor line, and red blood cells. Moreover, mass spectrometry analysis revealed that there are no proteins but several low molecular mass compounds and peptides. Three peptides, characterized as cryptides, and 14 low molecular mass compounds were found to be related to cytoskeleton reorganization, cell membrane expansion, and antioxidant/neuroprotective activity, which act together to increase neuritogenesis. After this evaluation, we conclude that the Cq extract is a promising tool for neuronal connection recovery, an essential condition for the treatment of neurodegenerative diseases.

show abstract

“…As reported, the neuroprotective action of estrogen appears to be closely linked to its antioxidant activity, which is due to its chemical properties as a hydrophobic phenolic molecule. [ 24,25 ] ER, which mediates protein synthesis, folding, and modification, is very sensitive to oxidative stress. ER responds to oxidative stress by unfolded protein response (UPR) to handle the increased need for protein folding or increased protein damage.…”

Section: Discussionmentioning

confidence: 99%

Inhibiting endoplasmic reticulum stress by activation of G‐protein‐coupled estrogen receptor to protect retinal astrocytes under hyperoxia

Wang

Chen

et al. 2020

J Biochem & Molecular Tox

View full text Add to dashboard Cite

Retinal vascularization is arrested at the early (hyperoxia) stage in retinopathy of prematurity (ROP), a leading cause of blindness in children. Estrogen was reported to alleviate ROP by inhibiting reactive oxygen species, the upstream signaling molecules of endoplasmic reticulum stress (ERS). Astrocytes have long been proposed to guide angiogenesis, because they form a reticular network that provides a substrate for migrating endothelial cells. However, the factors that control the vascularization of the immature retina and the therapeutic mechanism of estrogen in early ROP remain poorly understood. This study aimed to investigate the role of G‐protein‐coupled estrogen receptor (GPER), an estrogen receptor distributed in the endoplasmic reticulum (ER), in protecting retinal astrocytes under hyperoxia and the association with ERS. The results showed that GPER was widely expressed in retinal astrocytes. GPER activation increases cell viability, decreases apoptosis, and autophagy of retinal astrocytes, decreases inositol‐1,4,5‐triphosphate receptor activity, and increases Ca2+ concentration in ER of astrocytes under hyperoxia. GPER blockade reversed all of these changes. Together, our findings indicate that GPER can protect the survival of retinal astrocytes by inhibiting ERS under hyperoxia.

show abstract

Vastly extended drug release from poly(pro-17β-estradiol) materials facilitates in vitro neurotrophism and neuroprotection

Cited by 22 publications

References 65 publications

Aligned Fingolimod-Releasing Electrospun Fibers Increase Dorsal Root Ganglia Neurite Extension and Decrease Schwann Cell Expression of Promyelinating Factors

Aligned Fingolimod-Releasing Electrospun Fibers Increase Dorsal Root Ganglia Neurite Extension and Decrease Schwann Cell Expression of Promyelinating Factors

Box Jellyfish (Cnidaria, Cubozoa) Extract Increases Neuron’s Connection: A Possible Neuroprotector Effect

Inhibiting endoplasmic reticulum stress by activation of G‐protein‐coupled estrogen receptor to protect retinal astrocytes under hyperoxia

Contact Info

Product

Resources

About