Vani Maria Alves

Universidade de São Paulo

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Maria Célia Jamur

Universidade de São Paulo

Íd

Ísis do Carmo Kettelhut

Universidade de São Paulo

Adriana Andrade Batista Murashima

Universidade de São Paulo

MÂ

Miguel Ângelo Hyppolito

Universidade de São Paulo

Marcos Miranda de Araújo

Universidade de São Paulo

Marcelo Dias‐Baruffi

Universidade de São Paulo

Sean R. Stowell

Brigham and Women's Hospital

Luciane C. Alberici

Universidade de São Paulo

Lorena Rigo Gaspar

Universidade de São Paulo

Victor Bastos

Universidade Federal de Uberlândia

Cooperative Institutions

Universidade de São Paulo

Universidade de Ribeirão Preto

Clinics Hospital of Ribeirão Preto

Instituto de Neurociências e Comportamento

Universidade Brasil

Fundação de Amparo à Pesquisa do Estado de São Paulo

Hospital Universitário da Universidade de São Paulo

Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo

Universidade Federal do Triângulo Mineiro

Fundação Faculdade de Medicina

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Relative expression of KLK5 to LEKTI is associated with aggressiveness of oral squamous cell carcinoma

Translational Oncology (2020)

Márcia Gaião Alves Márcio Hideki Kodama Elaine Zayas Marcelino da Silva Bruno Belmonte Martinelli Gomes Rodrigo Alberto Alves da Silva

Oral squamous cell carcinoma (OSCC) remains a challenging cancer to treat despite all the advances of the last 50 years. Kallikrein 5 (KLK5) is among the serine proteases implicated in OSCC development. However, whether the activity of KLK5 promotes carcinogenesis is still controversial. Moreover, knowledge regarding the role of the KLK5 cognate inhibitor, Lympho-Epithelial Kazal-Type related Inhibitor (LEKTI), in OSCC is scarce. We have, thus, sought to investigate the importance of KLK5 and LEKTI expression in premalignant and malignant lesions of the oral cavity. KLK5 and LEKTI protein expression was evaluated in 301 human samples, which were comprised of non-malignant and malignant lesions of the oral cavity. Moreover, a bioinformatic analysis of the overall survival rate from 517 head and neck squamous cell carcinoma (HNSCC) samples was performed. Additionally, to mimic the uncovered KLK5 to serine peptidase inhibitor (SPINK5) imbalance, the KLK5 gene was abrogated in an OSCC cell line using CRISPR-Cas9 technology. The generated cell line was then used for in vivo and in vitro carcinogenesis related experiments. LEKTI was found to be statistically downregulated in OSCCs, with increased KLK5/SPINK5 mRNA ratio being associated with a shorter overall survival (p = 0.091). Indeed, disruption of KLK5 to SPINK5 balance through the generation of KLK5 null OSCC cells led to smaller xenografted tumors and statistically decreased proliferation rates following multiple time points of BrdU treatment in vitro. The association of increased enzyme/inhibitor ratio with poor prognosis indicates KLK5 to SPINK5 relative expression as an important prognostic marker in OSCC.

10.1016/j.tranon.2020.100970

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Citations (11)

In vivo photoprotective effects of cosmetic formulations containing UV filters, vitamins, Ginkgo biloba and red algae extracts

Journal of Photochemistry and Photobiology B Biology (2015)

Daiane Garcia Mercúrio Tais A. L. Wagemaker Vani Maria Alves Carolina Gomes Benevenuto Lorena Rigo Gaspar

Transepidermal water loss

Erythema

Hairless

10.1016/j.jphotobiol.2015.09.016

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Citations (69)

Morpho-physiological performance of Mikania glomerata Spreng. and Mikania laevigata Sch. Bip ex Baker plants under different light conditions

Hoehnea (2021)

Daniele Ribeiro Contin Eduardo Habermann Vani Maria Alves Carlos Alberto Martínez

ABSTRACT (Morpho-physiological performance of Mikania glomerata Spreng. and Mikania laevigata Sch. Bip ex Baker plants under different light conditions). In tropical and subtropical zones, lianas play important roles in the process of ecological succession. This study aims to evaluate the photosynthetic and morpho-physiological performance between two lianas species from Mikania genus in response to different levels of radiation: full sun (I0), 25% (I25), 50% (I50), and 75% (I75) retention of solar radiation flux. Plants grown under I75 showed a reduced net photosynthetic rate (A). We observed dynamic photoinhibition at I0 during hours of high irradiation and temperature. The highest and lowest leaf chlorophyll content occurred at I75 and I0, respectively, while carotenoids/total chlorophyll and leaf thickness increased under I0. Total dry mass was higher in plants grown at I0 and I25. However, A values and biomass production of Mikania laevigata were higher at I25, while for Mikania glomerata greater biomass accumulation was observed between I0-I50. Therefore, we concluded that M. laevigata and M. glomerata have different morpho-physiological performances under same the radiation conditions.

Liana

Morpho

Mikania micrantha

10.1590/2236-8906-74/2020

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Citations (1)

Crosstalk between hnRNP K and SET in ATRA‐induced differentiation in acute promyelocytic leukemia

FEBS Open Bio (2021)

Karina Stringhetta Padovani Renata N. Goto Lais Brigliadori Fugio Cristiana Bernadelli Garcia Vani Maria Alves

HnRNP K protein is a heterogeneous nuclear ribonucleoprotein which has been proposed to be involved in the leukemogenesis of acute promyelocytic leukemia (APL), as well as in differentiation induced by all‐trans retinoic acid (ATRA). We previously demonstrated a connection between SET and hnRNP K function in head and neck squamous cell carcinoma (HNSCC) cells related to splicing processing. The objective of this study was to characterize the participation of hnRNP K and SET proteins in ATRA‐induced differentiation in APL. We observed higher (5‐ to 40‐fold) levels of hnRNP K and SET mRNA in APL patients at the diagnosis phase compared with induction and maintenance phases. hnRNP K knockdown using short‐hairpin RNA led to cell death in ATRA‐sensitive NB4 and resistant NB4‐R2 cells by apoptosis with SET cleavage. In addition, hnRNP K knockdown increased granulocytic differentiation in APL cells, mainly in NB4‐R2 with ATRA. hnRNP K knockdown had an effect similar to that of treatment with U0126 (an meiosis‐specific serine/threonine protein kinase/ERK inhibitor), mainly in NB4‐R2 cells. SET knockdown in APL cells revealed that apoptosis induction in cells with hnRNP K knockdown occurred by SET cleavage rather than by reduction in SET protein. Transplantation of NB4‐R2 cells into nude mice confirmed that arsenic trioxide (ATO) combined with U0126 has higher potential against tumor progression when compared to ATO. Therefore, hnRNP K/SET and ERK are potential therapeutic targets for both antineoplastic leukemia therapy and relapsed APL patients with ATRA resistance.

Arsenic Trioxide

Promyelocytic leukemia protein

Tretinoin

Heterogeneous nuclear ribonucleoprotein

10.1002/2211-5463.13210

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The topical use of insulin accelerates the healing of traumatic Tympanic membrane perforations

The Laryngoscope (2015)

Marcos Miranda de Araújo Adriana Andrade Batista Murashima Vani Maria Alves Maria Célia Jamur Miguel Ângelo Hyppolito

Objective In recent years, there has been a tendency to search for regulatory substances that can optimize the healing process of perforated tympanic membranes (TMs). The purpose of this study was to determine the effects of using topical insulin on the healing process of traumatic TMs perforations. Study Design Experimental. Methods Tympanic membranes of 20 Wistar rats were perforated in two sections, anterior and posterior to the malleus. The rats were divided into two groups: control and insulin. The insulin group was treated with topical regular insulin. The TMs were histologically examined 3, 5, and 7 days after the perforation through a morphometric analysis of the epithelial layer thickness, perforation size, TM cross‐sectional area, semiquantitative and qualitative evaluation of the collagen production by polarization microscopy, and immunohistochemical evaluation of epithelial cells and myofibroblasts markers. Results Insulin accelerated the healing process of the perforated TMs ( P < 0.01); stimulated early thickening of the outer epithelial layer ( P < 0.01); contributed to a larger identification of the antipankeratin antibody as epithelial marker ( P < 0.05); and increased labeling of smooth muscle anti‐alpha‐actin antibody ( P < 0.05), indicating greater proliferation of myofibroblasts. When the topical insulin was used, it resulted in a greater formation of collagen tissue ( P < 0.05), with thicker and better‐organized collagen fibers ( P < 0.05). Conclusion Insulin accelerated the healing process of TMs traumatic perforations. Level of Evidence N/A. Laryngoscope , 126:156–162, 2016

Myofibroblast

Perforation

Malleus

10.1002/lary.25300

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Citations (17)

Endogenous galectin-3 is required for skeletal muscle repair

Glycobiology (2021)

Daniel Giuliano Cerri Lílian Cataldi Rodrigues Vani Maria Alves Juliano Machado Víctor Alexandre Félix Bastos

Skeletal muscle has the intrinsic ability to self-repair through a multifactorial process, but many aspects of its cellular and molecular mechanisms are not fully understood. There is increasing evidence that some members of the mammalian β-galactoside-binding protein family (galectins) are involved in the muscular repair process (MRP), including galectin-3 (Gal-3). However, there are many questions about the role of this protein on muscle self-repair. Here, we demonstrate that endogenous Gal-3 is required for: (i) muscle repair in vivo by using a chloride-barium myolesion mouse model and (ii) mouse primary myoblasts myogenic programming. Injured muscle from Gal-3 knockout mice (GAL3KO) showed persistent inflammation associated with compromised muscle repair and the formation of fibrotic tissue on the lesion site. In GAL3KO mice, osteopontin expression remained high even after 7 and 14 d of the myolesion, while Myoblast differentiation transcription factor (MyoD) and myogenin had decreased their expression. In GAL3KO mouse primary myoblast cell culture, Paired Box 7 (Pax7) detection seems to sustain even when cells are stimulated to differentiation and MyoD expression is drastically reduced. The detection and temporal expression levels of these transcriptional factors appear to be altered in Gal-3-deficient myoblast. Gal-3 expression in wild-type mice for GAL3KO states, both in vivo and in vitro, in sarcoplasm/cytoplasm and myonuclei; as differentiation proceeds, Gal-3 expression is drastically reduced, and its location is confined to the sarcolemma/plasma cell membrane. We also observed a change in the temporal-spatial profile of Gal-3 expression and muscle transcription factors levels during the myolesion. Overall, these results demonstrate that endogenous Gal-3 is required for the skeletal muscle repair process.

Sarcolemma

Mef2

10.1093/glycob/cwab071

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Citations (9)

Activation of adipose tissue glycerokinase contributes to increased white adipose tissue mass in mice fed a high-fat diet

Endocrine (2020)

Samyra Lopes Buzelle Franciele Przygodda Rafael Rossi-Valentim Graziella Nascimento Ferreira Maria Antonieta Rissato Garófalo

Hormone-sensitive lipase

Fatty acid synthesis

Adipose tissue macrophages

10.1007/s12020-020-02288-3

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Citations (7)

Spontaneous healing of the tympanic membrane after traumatic perforation in rats

Brazilian Journal of Otorhinolaryngology (2014)

Marcos Miranda de Araújo Adriana Andrade Batista Murashima Vani Maria Alves Maria Célia Jamur Miguel Ângelo Hyppolito

The most common etiologies of tympanic membrane perforation are infections and trauma.The objective of the present study was to assess the healing of traumatic tympanic membrane perforation in rats.The tympanic membrane from male Wistar rats was perforated in the anterior and posterior portions to the handle of the malleus. Five tympanic membranes were evaluated 3 days after tympanic perforation; 5 after 5 days; 5 after 7 days; 3 after 10 days; and 4 after 14 days. The tympanic membranes were submitted to histopathological evaluation after hematoxylin-eosin staining.Tympanic membrane closure occurred at about 7-10 days after injury and the healing process was complete by day 14. The proliferative activity of the outer epithelial layer was present close to the handle of the malleus and to the tympanic annulus.The spontaneous healing process of the tympanic membrane starts from the outer epithelial layer, with later healing of the lamina propria and the mucosal layer.

Malleus

Tympanic Membrane Perforation

Perforation

10.1016/j.bjorl.2014.05.014

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Citations (28)

Nuclear PKR in retinal neurons in the early stage of diabetic retinopathy in streptozotocin‑induced diabetic rats

Molecular Medicine Reports (2021)

Viviane Aline Oliveira Silva Nayara Delgado André Thais Amaral e Sousa Vani Maria Alves Ísis do Carmo Kettelhut

Retinal neuron apoptosis is a key component of diabetic retinopathy (DR), one of the most common complications of diabetes. Stress due to persistent hyperglycaemia and corresponding glucotoxicity represents one of the primary pathogenic mechanisms of diabetes and its complications. Apoptosis of retinal neurons serves a critical role in the pathogenesis of DR observed in patients with diabetes and streptozotocin (STZ)‑induced diabetic rats. Retinal neuron apoptosis occurs one month after STZ injection, which is considered the early stage of DR. The molecular mechanism involved in the suppression of retinal neuron apoptosis during the early stage of DR remains unclear. RNA‑dependent protein kinase (PKR) is a stress‑sensitive pro‑apoptotic kinase. Our previous study indicated that PKR‑associated protein X, a stress‑sensitive activator of PKR, is upregulated in the early stage of STZ‑induced diabetes. In order to assess the role of PKR in DR prior to apoptosis of retinal neurons, immunofluorescence and western blotting were performed to investigate the cellular localization and expression of PKR in the retina in the early stage of STZ‑induced diabetes in rats. PKR activity was indirectly assessed by expression levels of phosphorylated eukaryotic translation initiation factor 2α (p‑eIF2‑α) and the presence of apoptotic cells in the retina was investigated by TUNEL assay. The findings revealed that PKR was localized in the nucleus of retinal ganglion and inner nuclear layer cells from normal and diabetic rats. To the best of our knowledge, the present study is the first to demonstrate nuclear localization of PKR in retinal neurons. Immunofluorescence analysis demonstrated that PKR was expressed in the nuclei of retinal neurons at 3 and 6 days and its expression was decreased at 15 days after STZ treatment. In addition, p‑eIF2‑α expression and cellular localization followed the trend of PKR, suggesting that this pro‑apoptotic kinase was active in the nuclei of retinal neurons. These findings are consistent with the hypothesis that nuclear translocation of PKR may be a mechanism to sequester active PKR, thus preventing upregulation of cytosolic signalling pathways that induce apoptosis in retinal neurons. Apoptotic cells were not detected in the retina in the early stage of DR. A model was proposed to explain the mechanism by which apoptosis of retinal neurons by PKR is suppressed in the early stage of DR. The possible role of mitochondrial RNA (mtRNA) and Alu RNA in this phenomenon is also discussed since it was demonstrated that the cellular stress due to prolonged hyperglycaemia induces the release of mtRNA and transcription of Alu RNA. Moreover, it mtRNA activates PKR, whereas Alu RNA inhibits the activation of this protein kinase.

Protein kinase R

Inner nuclear layer

10.3892/mmr.2021.12253

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Citations (7)

Effect of different irradiance levels on anatomy and growth of two Malvaceae species during two seasons

Revista Brasileira de Botânica (2020)

Daniele Ribeiro Contin Eduardo Habermann Vani Maria Alves Carlos Alberto Martínez

Reforestation

Deforestation

Photosynthetically active radiation

10.1007/s40415-020-00609-4

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Citations (5)