Beatriz De Andrade Berti’s research while affiliated with State University of Campinas (UNICAMP) and other places

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Publications (2)

Figure 1. Effects of GA treatment in cell culture and in vivo. Experimental design of cell culture experiment using HaCaT, Primary human keratinocytes, and human fibroblast treated with different concentration of GA (a). MTT viability test results of Primary human keratinocytes with 2 days of Glutamic acid exposure (b). MTT viability test results of HaCaT with 2 days of Glutamic acid exposure (c). MTT viability test results of huma fibroblast with 2 days of Glutamic acid exposure (d). MTT viability test of primary keratinocytes in triplicate in 2 different experiments. MTT viability test of HaCaT keratinocytes in quadruplicate in 4 different experiments. MTT viability test of human fibroblast in quadruplicate in 2-3 different experiments. Immunostaining results of HaCaT keratinocytes treated with Glutamic acid 10 mM or 100 mM in DMEM compared to Control group treated with DMEM (g). Immunostaining results of HaCaT keratinocytes in triplicate in 4 different experiments, GA for 48 h and, finally, 3 h with BrdU, scale bar 50 μm. The proportion of BrdU-immunoreactive increased after exposure to GA 10 mM (f). Data is presented as mean ± SEM. N = 4 per group. p = 0.03 t-test Control versus GA 10 mM; p = 0.03 one-way ANOVA.
Figure 3. GA stimulates hair growth and increased BrdU + cells. Dose-response results of topical GA application on the dorsal region of mice with Vaseline (CTL) or 0.1%, 0.5%, 1% and 10% GA for 14 days (a-c). 5-6 animals per group. Hair growth effect after 14 days of GA treatment on the back of Swiss mice (a). Haematoxylin and Eosin (H&E) staining sample of the back of 14 day treated mice (hair follicle pointed with yellow arrows), scale bar 250 μm, samples from 3 different animals (b). Immunostaining results of skin samples treated 0.1%, 0.5%, 1%, and 10% Glutamic acid compared to Control group (Vaseline) (c). Immunostaining results of skin samples from 3 different animals, GA topical treatment for 14 days and, finally, 2 h with intraperitoneal BrdU. Yellow arrows indicate BrdU + cells.
Figure 4. Topical GA and blood vessel. Skin samples treated for 14 days with topical GA topical. Upsidedown back skin samples showing vessel differences between Vaseline (CTL) or 0.1%, 0.5%, 1% and 10% GA treatments (a). Quantification of blood vessel area after 14 days of vaseline (CTL) or 0.1%, 0.5%, 1% and 10% GA treatment (b). Gene expression of Hypoxia Inducible Factor 1 Subunit Alpha (Hif1a), Vascular Endothelial Growth Factor A (Vegf) and the Platelet and Endothelial Cell Adhesion Molecule 1 (Cd31) from full-thickness back skin after 14 days of GA treatment (c). GA receptor characterization in mice skin of different GA subunits (d-e). Immunostaining against NMDA Grin1, Grin2b, Grin2a and Grin2c GA receptor expressed in the epidermal layer of the skin of untreated mice (d-e). Yellow arrows indicate colocalization of K14 + Grin2b + cells (d). Quantification of positive BrdU epidermal and hair follicle cells of mice skin treated with vaseline (CTL) or 0.1%, 0.5%, 1% and 10% of GA (f). BrdU and quantitative PCR data are presented as mean ± SEM * < p 0.05 ANOVA. 5-6 animals per group.
Topical glutamic acid in mice. Experimental design of Swiss mice treated topically one at day with different concentration of GA for 14 days (a). Different GA concentrations (Control, 0.1%, 0.5%, 1% and 10% GA) for topical animal treatment were equal to 5.5 pH (b). RT-PCR of Bcl2, Bax, Casp9, F4/80, Mcp1, Il1β, Tnfα, Il10, Grin1 and Glast genes from skin samples after 14 days of GA treatment (c). GAPDH was used as endogenous control. Data is presented as mean ± SEM * < p 0.05 ANOVA. 5–6 animals per group.
Cross-species skin GA receptor landscape using single-cell RNA sequencing. Generation of glutamic acid receptor landscape using public data reveals GA distribution at single cell resolution in mice and humans (b–e). Schematic representation of the single-cell RNA sequencing analysis using publicly available datasets from mice and human epidermal layers (a). Human Epidermal Glutamate receptors (b) and transporter expression (c). Mice Epidermal Glutamate receptors (d) and transporter expression (e). Glutamic acid receptor and hair cycle Protein–Protein Interaction Network performed with STRING V11 (f). Glutamic acid and hair cycle interactome were retrieved with the data-mining toolkit STRING. Closer interactors of glutamic acid and hair cycle ontologies (GO:0007215 and GO:0042633) were selected and categorized by coloured nodes. Yellow arrows indicate shared shell interactors, red nodes indicate glutamate receptor signaling pathway genes and blue nodes hair cycle genes (f). Display of cropped blots quantified to confirm the Protein–Protein Interaction Network prediction (g–i). Western blot analysis of AKT Phosphorylation (g), phospho-CaMKII (h) and Fyn quantification (i). Full-length blots are presented in Supplementary Fig. 3. Western blot data are presented as mean ± SEM * < p 0.05 ANOVA. 4–5 animals per group.
Glutamic acid promotes hair growth in mice
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July 2021

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588 Reads

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26 Citations

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Beatriz De Andrade Berti

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Glutamic acid is the main excitatory neurotransmitter acting both in the brain and in peripheral tissues. Abnormal distribution of glutamic acid receptors occurs in skin hyperproliferative conditions such as psoriasis and skin regeneration; however, the biological function of glutamic acid in the skin remains unclear. Using ex vivo, in vivo and in silico approaches, we showed that exogenous glutamic acid promotes hair growth and keratinocyte proliferation. Topical application of glutamic acid decreased the expression of genes related to apoptosis in the skin, whereas glutamic acid increased cell viability and proliferation in human keratinocyte cultures. In addition, we identified the keratinocyte glutamic acid excitotoxic concentration, providing evidence for the existence of a novel skin signalling pathway mediated by a neurotransmitter that controls keratinocyte and hair follicle proliferation. Thus, glutamic acid emerges as a component of the peripheral nervous system that acts to control cell growth in the skin. These results raise the perspective of the pharmacological and nutritional use of glutamic acid to treat skin diseases.

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Glutamic acid promotes hair growth in mice

September 2020

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190 Reads

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1 Citation

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Beatriz de Andrade Berti

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[...]

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Glutamic Acid is the main excitatory neurotransmitter in neurons. Abnormal distributions of the glutamic acid receptors have been shown in hyper proliferative models such as psoriasis and skin regeneration. However, the biological function of glutamic acid in the skin remains unclear. Using ex vivo, in vivo and in silico approaches, we showed for the first time that exogenous glutamic acid promotes hair growth and keratinocyte proliferation. Topical application of glutamic acid decreased expression of genes related to apoptosis signaling in the skin. Also, we showed Glutamic acid increased viability and proliferation in cultured human keratinocyte. For the first time, we identified the excitotoxic GA concentration and we provided evidence for the existence of a novel skin signaling pathway mediated by a neurotransmitter controlling keratinocyte and hair follicle proliferation. In perspective, we anticipate our results could be the starting point to elucidate how exogenous glutamic acid from food intake or even endogenous GA from neuropsychiatric disorders modulate skin diseases.

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Citations (1)

... Glutamic acid (GA), the primary excitatory neurotransmitter in the mammalian central nervous system, has been found in the skin of various mammals, including humans, rats, and mice [12]. Studies discovered that GA enhances cell survival and proliferation [13]. ...

Reference:

Glutamic acid-loaded separable microneedle composite for long-acting hair regeneration treatment
Glutamic acid promotes hair growth in mice

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Beatriz De Andrade Berti

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