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9 pages, 5667 KiB

Open AccessArticle

Multiple Retinal Anomalies in Wfs1-Deficient Mice

by Arleta Waszczykowska, Agnieszka Zmysłowska, Marcin Braun, Marilin Ivask, Sulev Koks, Piotr Jurowski and Wojciech Młynarski

Diagnostics 2020, 10(9), 607; https://doi.org/10.3390/diagnostics10090607 - 19 Aug 2020

Cited by 5 | Viewed by 3821

Abstract

Background: Wolfram syndrome (WFS, OMIM: #222300) is an ultrarare autosomal recessive disorder characterized by diabetes insipidus, diabetes mellitus, optic nerve atrophy and deafness. It has been reported that the average retinal thickness in WFS patients decreases with the progression of the disease. Aim: [...] Read more.

Background: Wolfram syndrome (WFS, OMIM: #222300) is an ultrarare autosomal recessive disorder characterized by diabetes insipidus, diabetes mellitus, optic nerve atrophy and deafness. It has been reported that the average retinal thickness in WFS patients decreases with the progression of the disease. Aim: To investigate retinal thickness and wolframin expression disorders in Wolfram syndrome 1 gene knockout (Wfs1KO) mice compared to their wild-type (WT) littermates. Materials and methods: Both bulbs with optic nerves of three mice Wfs1WT and three Wfs1KO were taken for the histopathological examination. A strain of knockout mice with mutation in exon 8 was used. Results: No expression of wolframin protein in the retina and neurodegeneration of the optic nerve of Wfs1KO mice as compared among Wfs1WT mice was observed. The mean central retinal thickness was thinner and the retinal thickness/longitudinal diameter ratio was significantly lower in hte Wfs1KO as compared to the Wfs1WT mice. In four (67%) eyeballs of Wfs1KO mice, intra-retinal neovessels were observed. Conclusions: Wfs1KO mice retina with mutation in exon 8 present similar clinical features as patients with WFS in the form of reduced retinal thickness and neurodegeneration of the optic nerve. The presence of proliferative retinopathy observed in Wfs1KO mice requires further investigation. Full article

(This article belongs to the Special Issue Animal Models for Studying and Screening Human Diseases)

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10 pages, 2119 KiB

Open AccessArticle

Investigating Cardiac Morphological Alterations in a Pentylenetetrazol-Kindling Model of Epilepsy

by Enes Akyuz, Kristina Polat, Sukru Ates, Demet Unalmis, Adem Tokpinar, Seher Yilmaz, Emin Kaymak, Zuleyha Doganyigit and Chiara Villa

Diagnostics 2020, 10(6), 388; https://doi.org/10.3390/diagnostics10060388 - 9 Jun 2020

Cited by 13 | Viewed by 4611

Abstract

Epilepsy is a group of neurological disorders characterized by abnormal electrical activity in the central nervous system (CNS) and recurrent seizures representing the principal clinical manifestation. Sudden unexpected death in epilepsy (SUDEP) is the predominant cause of death in young epileptic patients. SUDEP [...] Read more.

Epilepsy is a group of neurological disorders characterized by abnormal electrical activity in the central nervous system (CNS) and recurrent seizures representing the principal clinical manifestation. Sudden unexpected death in epilepsy (SUDEP) is the predominant cause of death in young epileptic patients. SUDEP patients displayed an increased cardiovascular (CV) risk, probably due to an impaired autonomic control of CV functions, but the underlying mechanisms need to be explored yet. Therefore, we aimed to examine the cardiac morphological alterations in a pentylenetetrazol (PTZ)-kindled rat model, a well-established tool for studying chronic epilepsy. To complete this, the distance between the atria, between the atrium and ventricle were measured, the heart was weighed, and the pathological morphology of dissected hearts was analyzed by histological assessment with hematoxylin and eosin staining. A significantly decreased distance between atria and a significant increase in heart weight were observed in PTZ-kindled rats which interestingly also displayed increased hemorrhagic content when compared with controls. Our findings provided evidence that changes in cardiac morphology may be related to autonomic CV dysfunctions occurring during SUDEP while also opening up more avenues to better develop novel drugs for the treatment of this disorder. Full article

(This article belongs to the Special Issue Animal Models for Studying and Screening Human Diseases)

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11 pages, 3423 KiB

Open AccessArticle

Platelet-Rich Plasma Ameliorates Cyclophosphamide-Induced Acute Interstitial Cystitis/Painful Bladder Syndrome in a Rat Model

by Yung-Hsiang Chen, Kee-Ming Man, Wen-Chi Chen, Po-Len Liu, Kao-Sung Tsai, Ming-Yen Tsai, Yu-Tzu Wu and Huey-Yi Chen

Diagnostics 2020, 10(6), 381; https://doi.org/10.3390/diagnostics10060381 - 8 Jun 2020

Cited by 15 | Viewed by 3919

Abstract

Background: Interstitial cystitis/painful bladder syndrome (IC/PBS) could be treated to ameliorate urothelial injury. Here, we investigated the efficacy of intravesical instillation with platelet-rich plasma (PRP) and hyaluronic acid for acute IC/PBS. Methods: The effects of PRP and hyaluronic acid on the proliferation of [...] Read more.

Background: Interstitial cystitis/painful bladder syndrome (IC/PBS) could be treated to ameliorate urothelial injury. Here, we investigated the efficacy of intravesical instillation with platelet-rich plasma (PRP) and hyaluronic acid for acute IC/PBS. Methods: The effects of PRP and hyaluronic acid on the proliferation of normal human fibroblast cells (HFCs) were assessed. Additionally, thirty virgin female rats were randomized into five groups: group 1, saline-injected control; group 2, cyclophosphamide (CYP) plus intravesical instillation with normal saline; group 3, CYP plus intravesical instillation with hyaluronic acid (1 mg/mL); group 4, CYP plus intravesical instillation with PRP; and group 5, CYP plus intravesical instillation with PRP plus hyaluronic acid. A cystometry and histological assessments were performed. The expression of cell junction-associated protein zonula occludens-2 (ZO-2) and inflammatory cytokine interleukin 6 (IL-6) was also measured. Results: Low dose PRP increased proliferation in HFCs. The acute IC/PBS rats showed significantly lower voiding interval values. Voiding interval values were significantly higher in the CYP plus intravesical instillation with PRP group than in the CYP-induced acute IC/PBS group. Additionally, the expression of ZO-2 was increased and IL-6 was decreased in the CYP plus intravesical instillation with PRP group compared with the CYP-induced acute IC/PBS group. Conclusion: These findings suggest that PRP modulate urothelial repair, which ameliorate the increase in urination frequency in rats treated with CYP. Overall, PRP may confer potential benefits by acting as urothelial repair modulators. Full article

(This article belongs to the Special Issue Animal Models for Studying and Screening Human Diseases)

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17 pages, 2709 KiB

Open AccessArticle

MicroRNA Expression Profile Changes after Cardiopulmonary Bypass and Ischemia/Reperfusion-Injury in a Porcine Model of Cardioplegic Arrest

by Attila Kiss, Stefan Heber, Anne-Margarethe Kramer, Matthias Hackl, Susanna Skalicky, Seth Hallström, Bruno K. Podesser and David Santer

Diagnostics 2020, 10(4), 240; https://doi.org/10.3390/diagnostics10040240 - 21 Apr 2020

Cited by 9 | Viewed by 3489

Abstract

Identification of microRNAs (miRNA) associated with cardiopulmonary bypass, cardiac arrest and subsequent myocardial ischemia/reperfusion may unravel novel therapeutic targets and biomarkers. The primary aim of the present study was to investigate the effects of cardiopulmonary bypass and temperature of cardioplegic arrest on myocardial [...] Read more.

Identification of microRNAs (miRNA) associated with cardiopulmonary bypass, cardiac arrest and subsequent myocardial ischemia/reperfusion may unravel novel therapeutic targets and biomarkers. The primary aim of the present study was to investigate the effects of cardiopulmonary bypass and temperature of cardioplegic arrest on myocardial miRNA profile in pigs’ left ventricular tissue. We employed next-generation sequencing to analyse miRNA profiles in the following groups: (1) hearts were arrested with antegrade warm St Thomas Hospital No. 2 (STH2) cardioplegia (n = 5; STH2-warm, 37 °C) and (2) cold STH2 (n = 6; STH2-cold, 4 °C) cardioplegia. Sixty min of ischemia was followed by 60 min of on-pump reperfusion with an additional 90 min of off-pump reperfusion. In addition, two groups without cardiac arrest (off-pump and on-pump group; n = 3, respectively) served as additional controls. STH2-warm and STH2-cold cardioplegia revealed no hemodynamic differences. In contrast, coronary venous creatine kinase-myocardial band (CK-MB) levels were significantly lower in pigs receiving STH2-warm cardioplegia (p < 0.05). Principal component analysis revealed that cardiopulmonary bypass and cardioplegic arrest markedly affected miRNAs in left ventricular tissue. Accordingly, ssc-miR-122, ssc-miR-10a-5p, ssc-miR-193a-3p, ssc-miR-499-3p, ssc-miR-374a-5p, ssc-miR-345-5p, ssc-miR-142-3p, ssc-miR-424-5p, ssc-miR-545-3p, ssc-miR-30b-5p, ssc-miR-145-5p, ssc-miR-374b-5p and ssc-miR-139-3p were differently regulated by cardiopulmonary bypass (false discovery rate (FDR) < 0.05 versus off-pump group). However, only ssc-miR-451 was differently expressed between STH2-warm and STH2-cold (FDR < 0.05). These data demonstrate for the first time that cardiopulmonary bypass and temperature of cardioplegic solution affected the expression of miRNAs in left ventricular tissue. In conclusion, specific miRNAs are potential therapeutic targets for limiting ischemia-reperfusion injury in patients undergoing cardiac surgery. Full article

(This article belongs to the Special Issue Animal Models for Studying and Screening Human Diseases)

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10 pages, 1673 KiB

Open AccessArticle

Diet-Induced Rat Model of Gradual Development of Non-Alcoholic Fatty Liver Disease (NAFLD) with Lipopolysaccharides (LPS) Secretion

by Dominika Maciejewska, Agnieszka Łukomska, Karolina Dec, Karolina Skonieczna-Żydecka, Izabela Gutowska, Marta Skórka-Majewicz, Daniel Styburski, Kamila Misiakiewicz-Has, Anna Pilutin, Joanna Palma, Katarzyna Sieletycka, Wojciech Marlicz and Ewa Stachowska

Diagnostics 2019, 9(4), 205; https://doi.org/10.3390/diagnostics9040205 - 27 Nov 2019

Cited by 30 | Viewed by 4782

Abstract

Background: Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver disorders in industrialized Western countries. The prevalence of the disease is estimated to range from 4% to 46% worldwide. The aim of study was to develop an animal model with [...] Read more.

Background: Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver disorders in industrialized Western countries. The prevalence of the disease is estimated to range from 4% to 46% worldwide. The aim of study was to develop an animal model with gradual NAFLD development. Methods: Sprague-Dawley rats were fed a high-fat and high-cholesterol (HFHCh) diet. The rats from the study and control groups were sacrificed after 2, 4, 8, 12, 16, and 20 weeks of dietary exposure. Results: Analysis of biochemical parameters showed that after only two weeks, ALT and cholesterol concentration in serum were elevated. After 4 weeks, TNF-α and HOMA-IR were significantly higher compared to the control group. NAFLD progression started after 12 weeks of diet-weight gain and increased LPS secretions were noticed. During the experiment, rats induced steatosis (from stage 0/1 after 4 weeks to stage 2/3 after 20 weeks), inflammation (from stage 0/1 after 4 weeks to stage 1/2 after 20 weeks), and fibrosis (from stage 1 after 12 weeks to stage 2 after 20 weeks). Conclusion: We can assume that the presented model based on the HFHCh diet induced gradual development of NAFLD. We confirmed that the animal NAFLD model increases LPS secretions during disease progression. Full article

(This article belongs to the Special Issue Animal Models for Studying and Screening Human Diseases)

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Review

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31 pages, 544 KiB

Open AccessReview

Animal Models of Depression: What Can They Teach Us about the Human Disease?

by Maria Becker, Albert Pinhasov and Asher Ornoy

Diagnostics 2021, 11(1), 123; https://doi.org/10.3390/diagnostics11010123 - 14 Jan 2021

Cited by 91 | Viewed by 20855

Abstract

Depression is apparently the most common psychiatric disease among the mood disorders affecting about 10% of the adult population. The etiology and pathogenesis of depression are still poorly understood. Hence, as for most human diseases, animal models can help us understand the pathogenesis [...] Read more.

Depression is apparently the most common psychiatric disease among the mood disorders affecting about 10% of the adult population. The etiology and pathogenesis of depression are still poorly understood. Hence, as for most human diseases, animal models can help us understand the pathogenesis of depression and, more importantly, may facilitate the search for therapy. In this review we first describe the more common tests used for the evaluation of depressive-like symptoms in rodents. Then we describe different models of depression and discuss their strengths and weaknesses. These models can be divided into several categories: genetic models, models induced by mental acute and chronic stressful situations caused by environmental manipulations (i.e., learned helplessness in rats/mice), models induced by changes in brain neuro-transmitters or by specific brain injuries and models induced by pharmacological tools. In spite of the fact that none of the models completely resembles human depression, most animal models are relevant since they mimic many of the features observed in the human situation and may serve as a powerful tool for the study of the etiology, pathogenesis and treatment of depression, especially since only few patients respond to acute treatment. Relevance increases by the fact that human depression also has different facets and many possible etiologies and therapies. Full article

(This article belongs to the Special Issue Animal Models for Studying and Screening Human Diseases)

36 pages, 2226 KiB

Open AccessReview

Spontaneous and Induced Animal Models for Cancer Research

by Anca Onaciu, Raluca Munteanu, Vlad Cristian Munteanu, Diana Gulei, Lajos Raduly, Richard-Ionut Feder, Radu Pirlog, Atanas G. Atanasov, Schuyler S. Korban, Alexandru Irimie and Ioana Berindan-Neagoe

Diagnostics 2020, 10(9), 660; https://doi.org/10.3390/diagnostics10090660 - 31 Aug 2020

Cited by 54 | Viewed by 15393

Abstract

Considering the complexity of the current framework in oncology, the relevance of animal models in biomedical research is critical in light of the capacity to produce valuable data with clinical translation. The laboratory mouse is the most common animal model used in cancer [...] Read more.

Considering the complexity of the current framework in oncology, the relevance of animal models in biomedical research is critical in light of the capacity to produce valuable data with clinical translation. The laboratory mouse is the most common animal model used in cancer research due to its high adaptation to different environments, genetic variability, and physiological similarities with humans. Beginning with spontaneous mutations arising in mice colonies that allow for pursuing studies of specific pathological conditions, this area of in vivo research has significantly evolved, now capable of generating humanized mice models encompassing the human immune system in biological correlation with human tumor xenografts. Moreover, the era of genetic engineering, especially of the hijacking CRISPR/Cas9 technique, offers powerful tools in designing and developing various mouse strains. Within this article, we will cover the principal mouse models used in oncology research, beginning with behavioral science of animals vs. humans, and continuing on with genetically engineered mice, microsurgical-induced cancer models, and avatar mouse models for personalized cancer therapy. Moreover, the area of spontaneous large animal models for cancer research will be briefly presented. Full article

(This article belongs to the Special Issue Animal Models for Studying and Screening Human Diseases)

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12 pages, 1119 KiB

Open AccessReview

Animal Models for Studying Stone Disease

by Szu-Ju Chen, Kun-Yuan Chiu, Huey-Yi Chen, Wei-Yong Lin, Yung-Hsiang Chen and Wen-Chi Chen

Diagnostics 2020, 10(7), 490; https://doi.org/10.3390/diagnostics10070490 - 18 Jul 2020

Cited by 10 | Viewed by 3957

Abstract

Animals have stone disease too. There are several animal models for the research of human stone disease. Rodents are the most frequently used for stone research, although they are not prone to forming crystals in the kidneys. Ethylene glycol (EG), sodium oxalate and [...] Read more.

Animals have stone disease too. There are several animal models for the research of human stone disease. Rodents are the most frequently used for stone research, although they are not prone to forming crystals in the kidneys. Ethylene glycol (EG), sodium oxalate and l-hydroxyproline are common lithogenic agents. Dogs and pigs were also reported as a study animal for stone disease. However, the breeding costs and body size are too high. The most-used genetic study animal for stone disease was the mouse, but it was high-cost. Calcium oxalate (CaOx) crystals can also be light microscopically observed in the Malphigian tubules of Drosophila melanogaster, induced by adding EG to the food. Genetic studies of flies can be done by cross-breeding, and this has a lower cost than using mice. The fly model also has several advantages, including minimal breeding equipment, the fact that it is easier to reach larger numbers in a short time with flies, that crystals can be observed under microscopy, and that they allow genetic study. We suggest the fly will be an ideal animal model for stone research in the future. Full article

(This article belongs to the Special Issue Animal Models for Studying and Screening Human Diseases)

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11 pages, 209 KiB

Open AccessReview

Animal Models of Post-Traumatic Epilepsy

by Kristin A. Keith and Jason H. Huang

Diagnostics 2020, 10(1), 4; https://doi.org/10.3390/diagnostics10010004 - 19 Dec 2019

Cited by 15 | Viewed by 3750

Abstract

Traumatic brain injury is the leading cause of morbidity and mortality worldwide, with the incidence of post-traumatic epilepsy increasing with the severity of the head injury. Post-traumatic epilepsy (PTE) is defined as a recurrent seizure disorder secondary to trauma to the brain and [...] Read more.

Traumatic brain injury is the leading cause of morbidity and mortality worldwide, with the incidence of post-traumatic epilepsy increasing with the severity of the head injury. Post-traumatic epilepsy (PTE) is defined as a recurrent seizure disorder secondary to trauma to the brain and has been described as one of the most devastating complications associated with TBI (Traumatic Brain Injury). The goal of this review is to characterize current animal models of PTE and provide succinct protocols for the development of each of the currently available animal models. The development of translational and effective animal models for post-traumatic epilepsy is critical in both elucidating the underlying pathophysiology associated with PTE and providing efficacious clinical breakthroughs in the management of PTE. Full article

(This article belongs to the Special Issue Animal Models for Studying and Screening Human Diseases)

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