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Biomedicines
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Apoptosis—50 Years after Its Discovery
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Apoptosis—50 Years after Its Discovery

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (31 July 2022) | Viewed by 19194

Special Issue Editors

Prof. Dr. Cecilia M. P. Rodrigues

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Guest Editor
Research institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, University of Lisbon, Lisbon, Portugal
Interests: Biomarkers and therapeutics; Cell function and fate; Liver, gut and neurodegenerative diseases; Molecular targets
Special Issues, Collections and Topics in MDPI journals
Dr. Fernando Capela e Silva

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Guest Editor
1. Department of Medical and Health Sciences, School of Health and Human Development, University of Évora, 7000-671 Évora, Portugal
2. Mediterranean Institute for Agriculture, Environment and Development (MED), University of Évora, 7000-671 Évora, Portugal
Interests: biology of oral tissues; eating behavior and its effects on the health of people and populations; food, health and society and the “One Health” approach
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Apoptosis is a type of programmed cell death found in animals, first described in 1972 [Kerr et al. 1972]. As the authors mentioned in the original article, “The term apoptosis is proposed for a hitherto little recognized mechanism of controlled cell deletion, which appears to play a complementary but opposite role to mitosis in the regulation of animal cell populations”. It is known that apoptosis is involved in cell turnover in many healthy adult tissues, in both physiological involution and atrophy of various tissues and organs—such as in the female reproductive cycle and in the renewal of the epidermis and gastrointestinal mucosa—and is responsible for the focal elimination of cells during normal embryonic development—for example, during endochondral ossification and palatal fusion. On the other hand, anomalies in the regulation of cell death can play a significant role in some diseases including cancer and neurodegenerative diseases such as Parkinson's and Alzheimer's diseases. Whereas some situations are associated with insufficient apoptosis, others have an excess of apoptosis. Cell death by apoptosis can also be induced by noxious agents, in both the embryo and the adult animal.

Fifty years after its discovery (2022), we think that a Special Issue about the role of apoptosis in health and disease would be interesting, highlighting the balances/imbalances between apoptosis and the cell cycle and other associated events for the maintenance of tissue homeostasis, namely, differentiation, migration, and programmed cell clearance. For this Special Issue authors are invited to review recent work or submit original studies in all areas of cell death research, with an emphasis on the aforementioned balances/imbalances between apoptosis and other cellular processes and on novel physiological and pathological functions or regulatory mechanisms in normal tissues and in various diseases.

Kerr JF, Wyllie AH, Currie AR 1972 Apoptosis: a basic biological phenomenon with wide-ranging implications in tissue kinetics Br. J. Cancer 26 239–57.

Prof. Dr. Cecilia Rodrigues
Prof. Fernando Capela e Silva
Guest Editors

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Published Papers (6 papers)

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Editorial

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3 pages, 205 KiB  
Editorial
Apoptosis—50 Years after Its Discovery
by Fernando Capela e Silva and Cecília M. P. Rodrigues
Biomedicines 2023, 11(4), 1196; https://doi.org/10.3390/biomedicines11041196 - 18 Apr 2023
Cited by 4 | Viewed by 1320
Abstract
Apoptosis is a programmed cell death routine that plays an essential role in several biological processes, namely, embryonic development, tissue homeostasis, and immune response [...] Full article
(This article belongs to the Special Issue Apoptosis—50 Years after Its Discovery)

Research

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21 pages, 2741 KiB  
Article
Pulegone and Eugenol Oral Supplementation in Laboratory Animals: Results from Acute and Chronic Studies
by Carla M. Ribeiro-Silva, Ana I. Faustino-Rocha, Rui M. Gil da Costa, Rui Medeiros, Maria J. Pires, Isabel Gaivão, Adelina Gama, Maria J. Neuparth, Joana V. Barbosa, Francisco Peixoto, Fernão D. Magalhães, Margarida M. S. M. Bastos and Paula A. Oliveira
Biomedicines 2022, 10(10), 2595; https://doi.org/10.3390/biomedicines10102595 - 17 Oct 2022
Cited by 12 | Viewed by 3174
Abstract
Essential oils are natural compounds used by humans for scientific purposes due to their wide range of properties. Eugenol is mostly present in clove oil, while pulegone is the main constituent of pennyroyal oil. To guarantee the safe use of eugenol and pulegone [...] Read more.
Essential oils are natural compounds used by humans for scientific purposes due to their wide range of properties. Eugenol is mostly present in clove oil, while pulegone is the main constituent of pennyroyal oil. To guarantee the safe use of eugenol and pulegone for both humans and animals, this study addressed, for the first time, the effects of these compounds, at low doses (chronic toxicity) and high doses (acute toxicity), in laboratory animals. Thirty-five FVB/n female mice were randomly assigned to seven groups (n = 5): group I (control, non-additive diet); group II (2.6 mg of eugenol + 2.6 mg of pulegone); group III (5.2 mg of eugenol + 5.2 mg of pulegone); group IV (7.8 mg of eugenol + 7.8 mg of pulegone); group V (7.8 mg of eugenol); group VI (7.8 mg of pulegone); and group VII (1000 mg of eugenol + 1000 mg of pulegone). The compounds were administered in the food. Groups I to VI were integrated into the chronic toxicity study, lasting 28 days, and group VII was used in the acute toxicity study, lasting 7 days. Animals were monitored to assess their general welfare. Water and food intake, as well as body weight, were recorded. On the 29th day, all animals were euthanized by an overdose of ketamine and xylazine, and a complete necropsy was performed. Blood samples were collected directly from the heart for microhematocrit and serum analysis, as well as for comet assay. Organs were collected, weighed, and fixed in formaldehyde for further histological analysis and enzymatic assay. Eugenol and pulegone induced behavioral changes in the animals, namely in the posture, hair appearance and grooming, and in mental status. These compounds also caused a decrease in the animals’ body weight, as well as in the food and water consumption. A mortality rate of 20% was registered in the acute toxicity group. Both compounds modulated the serum levels of triglycerides and alanine aminotransferase. Eugenol and pulegone induced genetic damage in all animals. Eugenol increased the activity of the CAT enzyme. Both compounds increased the GR enzyme at the highest dose. Moreover, pulegone administered as a single compound increased the activity of the GST enzyme. Histopathological analysis revealed inflammatory infiltrates in the lungs of groups II, III, and IV. The results suggest that eugenol and pulegone may exert beneficial or harmful effects, depending on the dose, and if applied alone or in combination. Full article
(This article belongs to the Special Issue Apoptosis—50 Years after Its Discovery)
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20 pages, 5924 KiB  
Article
Characterization of the Tumor Microenvironment and the Biological Processes with a Role in Prostatic Tumorigenesis
by Cristina-Anita Ionescu, Mariana Aschie, Elena Matei, Georgeta Camelia Cozaru, Mariana Deacu, Anca Florentina Mitroi, Gabriela Isabela Baltatescu, Antonela-Anca Nicolau, Laura Mazilu, Liliana Ana Tuta, Ionut Ciprian Iorga, Alina Stanigut and Manuela Enciu
Biomedicines 2022, 10(7), 1672; https://doi.org/10.3390/biomedicines10071672 - 12 Jul 2022
Cited by 7 | Viewed by 2390
Abstract
Prostate intratumoral heterogeneity, driven by epithelial–mesenchymal plasticity, contributes to the limited treatment response, and it is therefore necessary to use the biomarkers to improve patient prognostic survival. We aimed to characterize the tumor microenvironment (T lymphocyte infiltration, intratumoral CD34, and KI-67 expressions) by [...] Read more.
Prostate intratumoral heterogeneity, driven by epithelial–mesenchymal plasticity, contributes to the limited treatment response, and it is therefore necessary to use the biomarkers to improve patient prognostic survival. We aimed to characterize the tumor microenvironment (T lymphocyte infiltration, intratumoral CD34, and KI-67 expressions) by immunohistochemistry methods and to study the biological mechanisms (cell cycle, cell proliferation by adhesion glycoproteins, cell apoptosis) involved in the evolution of the prostate tumor process by flow-cytometry techniques. Our results showed that proliferative activity (S-phase) revealed statistically significant lower values of prostate adenocarcinoma (PCa) and benign prostatic hyperplasia (BPH) reported at non-malignant adjacent cell samples (PCa 4.32 ± 4.91; BPH 2.35 ± 1.37 vs. C 10.23 ± 0.43, p < 0.01). Furthermore, 68% of BPH cases and 88% of patients with PCa had aneuploidy. Statistically increased values of cell proliferation (CD34+ CD61+) were observed in prostate adenocarcinoma and hyperplasia cases reported to non-malignant adjacent cell samples (PCa 28.79 ± 10.14; BPH 40.65 ± 11.88 vs. C 16.15 ± 2.58, p < 0.05). The CD42b+ cell population with a role in cell adhesion, and metastasis had a significantly increased value in PCa cases (38.39 ± 11.23) reported to controls (C 26.24 ± 0.62, p < 0.01). The intratumoral expression of CD34 showed a significantly increased pattern of PCa tissue samples reported to controls (PCa 26.12 ± 6.84 vs. C 1.50 ± 0.70, p < 0.01). Flow cytometric analysis of the cell cycle, apoptosis, and adhesion glycoproteins with a critical role in tumoral cell proliferation, T cell infiltrations, Ki-67, and CD 34 expressions by IHC methods are recommended as techniques for the efficient means of measurement for adenocarcinoma and hyperplasia prostate tissue samples and should be explored in the future. Full article
(This article belongs to the Special Issue Apoptosis—50 Years after Its Discovery)
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17 pages, 3080 KiB  
Article
SERTAD1 Sensitizes Breast Cancer Cells to Doxorubicin and Promotes Lysosomal Protein Biosynthesis
by Hai Anh Nguyen, Son Hai Vu, Samil Jung, Beom Suk Lee, Thi Ngoc Quynh Nguyen, Hyojeong Lee, Hye-gyeong Lee, Davaajargal Myagmarjav, Taeyeon Jo, Yeongseon Choi and Myeong-Sok Lee
Biomedicines 2022, 10(5), 1148; https://doi.org/10.3390/biomedicines10051148 - 17 May 2022
Cited by 2 | Viewed by 2832
Abstract
Acquired chemoresistance of tumor cells is an unwanted consequence of cancer treatment. Overcoming chemoresistance is particularly important for efficiently improving cancer therapies. Here, using multiple lines of evidence, we report the suppressive role of SERTAD1 in apoptosis/anoikis. Among various breast cancer cell lines, [...] Read more.
Acquired chemoresistance of tumor cells is an unwanted consequence of cancer treatment. Overcoming chemoresistance is particularly important for efficiently improving cancer therapies. Here, using multiple lines of evidence, we report the suppressive role of SERTAD1 in apoptosis/anoikis. Among various breast cancer cell lines, higher SERTAD1 expression was found in MCF7 and MDA-MB-231 in suspension than in adherent cell culture. We revealed an unexpected phenomenon that different types of cell deaths were induced in response to different doses of doxorubicin (Dox) in breast cancer cells, presumably via lysosomal membrane permeabilization. A low dose of Dox highly activated autophagy, while a high dose of the chemotherapy induced apoptosis. Inhibition of SERTAD1 promoted the sensitivity of breast cancer cells to Dox and paclitaxel, leading to a significant reduction in tumor volumes of xenograft mice. Simultaneously targeting cancer cells with Dox and autophagy inhibition successfully induced higher apoptosis/anoikis. The novel role of SERTAD1 in maintaining cellular homeostasis has also been suggested in which lysosomal contents, including LAMP1, LAMP2, CTSB, and CTSD, were reduced in SERTAD1-deficient cells. Full article
(This article belongs to the Special Issue Apoptosis—50 Years after Its Discovery)
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40 pages, 6643 KiB  
Article
Association of Caspase 3 Activation and H2AX γ Phosphorylation in the Aging Brain: Studies on Untreated and Irradiated Mice
by Nadia Gionchiglia, Alberto Granato, Adalberto Merighi and Laura Lossi
Biomedicines 2021, 9(9), 1166; https://doi.org/10.3390/biomedicines9091166 - 6 Sep 2021
Cited by 13 | Viewed by 3403
Abstract
Phosphorylation of H2AX is a response to DNA damage, but γH2AX also associates with mitosis and/or apoptosis. We examined the effects of X-rays on DNA integrity to shed more light on the significance of H2AX phosphorylation and its relationship with activation of caspase [...] Read more.
Phosphorylation of H2AX is a response to DNA damage, but γH2AX also associates with mitosis and/or apoptosis. We examined the effects of X-rays on DNA integrity to shed more light on the significance of H2AX phosphorylation and its relationship with activation of caspase 3 (CASP3), the main apoptotic effector. After administration of the S phase marker BrdU, brains were collected from untreated and irradiated (10 Gray) 24-month-old mice surviving 15 or 30 min after irradiation. After paraffin embedding, brain sections were single- or double-stained with antibodies against γH2AX, p53-binding protein 1 (53BP1) (which is recruited during the DNA damage response (DDR)), active CASP3 (cCASP3), 5-Bromo-2-deoxyuridine (BrdU), and phosphorylated histone H3 (pHH3) (which labels proliferating cells). After statistical analysis, we demonstrated that irradiation not only induced a robust DDR with the appearance of γH2AX and upregulation of 53BP1 but also that cells with damaged DNA attempted to synthesize new genetic material from the rise in BrdU immunostaining, with increased expression of cCASP3. Association of γH2AX, 53BP1, and cCASP3 was also evident in normal nonirradiated mice, where DNA synthesis appeared to be linked to disturbances in DNA repair mechanisms rather than true mitotic activity. Full article
(This article belongs to the Special Issue Apoptosis—50 Years after Its Discovery)
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Review

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23 pages, 2298 KiB  
Review
Apoptosis and (in) Pain—Potential Clinical Implications
by Hugo Ribeiro, Ana Bela Sarmento-Ribeiro, José Paulo Andrade and Marília Dourado
Biomedicines 2022, 10(6), 1255; https://doi.org/10.3390/biomedicines10061255 - 27 May 2022
Cited by 15 | Viewed by 3749
Abstract
The deregulation of apoptosis is involved in the development of several pathologies, and recent evidence suggests that apoptosis may be involved in chronic pain, namely in neuropathic pain. Neuropathic pain is a chronic pain state caused by primary damage or dysfunction of the [...] Read more.
The deregulation of apoptosis is involved in the development of several pathologies, and recent evidence suggests that apoptosis may be involved in chronic pain, namely in neuropathic pain. Neuropathic pain is a chronic pain state caused by primary damage or dysfunction of the nervous system; however, the details of the molecular mechanisms have not yet been fully elucidated. Recently, it was found that nerve endings contain transient receptor potential (TRP) channels that sense and detect signals released by injured tissues and respond to these damage signals. TRP channels are similar to the voltage-gated potassium channels or nucleotide-gated channels that participate in calcium and magnesium homeostasis. TRP channels allowing calcium to penetrate into nerve terminals can activate apoptosis, leading to nerve terminal destruction. Further, some TRPs are activated by acid and reactive oxygen species (ROS). ROS are mainly produced in the mitochondrial respiratory chain, and an increase in ROS production and/or a decrease in the antioxidant network may induce oxidative stress (OS). Depending on the OS levels, they can promote cellular proliferation and/or cell degeneration or death. Previous studies have indicated that proinflammatory cytokines, such as tumor necrosis factor-α (TNF-α), play an important role in the peripheral mediation of neuropathic pain. This article aims to perform a review of the involvement of apoptosis in pain, particularly the role of OS and neuroinflammation, and the clinical relevance of this knowledge. The potential discovery of new biomarkers and therapeutic targets can result in the development of more effective and targeted drugs to treat chronic pain, namely neuropathic pain. Highlights: Oxidative stress and neuroinflammation can activate cell signaling pathways that can lead to nerve terminal destruction by apoptosis. These could constitute potential new pain biomarkers and targets for therapy in neuropathic pain. Full article
(This article belongs to the Special Issue Apoptosis—50 Years after Its Discovery)
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