Önen, Selin

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Profile URL
https://hdl.handle.net/20.500.14411/8366
Name Variants
Selin, Önen
Önen,S.
Önen, Selin
O., Selin
Selin, Onen
S.,Önen
O.,Selin
S.,Onen
Onen,S.
Ö.,Selin
Onen, Selin
S., Onen
Job Title
Araştırma Görevlisi
Email Address
selin.onen@atilim.edu.tr
Main Affiliation
Basic Sciences
Status
Former Staff
Website
ORCID ID
Scopus Author ID
Turkish CoHE Profile ID
Google Scholar ID
WoS Researcher ID

Sustainable Development Goals

2

ZERO HUNGER
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0

Research Products

14

LIFE BELOW WATER
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0

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17

PARTNERSHIPS FOR THE GOALS
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0

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5

GENDER EQUALITY
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0

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16

PEACE, JUSTICE AND STRONG INSTITUTIONS
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0

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8

DECENT WORK AND ECONOMIC GROWTH
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0

Research Products

4

QUALITY EDUCATION
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0

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6

CLEAN WATER AND SANITATION
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1

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7

AFFORDABLE AND CLEAN ENERGY
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0

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10

REDUCED INEQUALITIES
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0

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11

SUSTAINABLE CITIES AND COMMUNITIES
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1

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9

INDUSTRY, INNOVATION AND INFRASTRUCTURE
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0

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1

NO POVERTY
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0

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3

GOOD HEALTH AND WELL-BEING
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4

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12

RESPONSIBLE CONSUMPTION AND PRODUCTION
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0

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13

CLIMATE ACTION
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15

LIFE ON LAND
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This researcher does not have a Scopus ID.
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Scholarly Output

11

Articles

7

Views / Downloads

1/0

Supervised MSc Theses

0

Supervised PhD Theses

0

WoS Citation Count

90

Scopus Citation Count

96

WoS h-index

5

Scopus h-index

5

Patents

0

Projects

0

WoS Citations per Publication

8.18

Scopus Citations per Publication

8.73

Open Access Source

4

Supervised Theses

0

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JournalCount
Stem Cell Research & Therapy2
American Journal of Rhinology & Allergy1
Journal of Assisted Reproduction and Genetics1
Journal of Hazardous Materials1
Progress In Electromagnetics Research Symposium (PIERS) -- AUG 19-23, 2012 -- Moscow, RUSSIA1
Current Page: 1 / 2

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Author: Gizer, MerveHas files: false

Scholarly Output Search Results

Now showing 1 - 3 of 3
  • Thumbnail Image
    Article
    Citation - WoS: 1
    Citation - Scopus: 2
    Cannabinoid Receptor Ligands Modulate Fibrosis and Inflammation in Idiopathic Pulmonary Fibrosis: a Preliminary Study
    (Tubitak Scientific & Technological Research Council Turkey, 2024) Kose, Sevil; Onen, Selin; Gizer, Merve; Boduroglu, Esin; Gonullu, Ugur; Korkusuz, Petek
    Background/aim: No specific pharmacological treatment regimen for idiopathic pulmonary fibrosis (IPF) exists. Therefore, new antiinflammatory therapeutic strategies are needed. Cannabinoids (CBs), known for their inflammation-modulating and antifibrotic effects, may be potential medication candidates for treating IPF. We aim to evaluate the inflammation-modulating and antifibrotic effects of CB receptor (CBR) agonists and antagonists in lipopolysaccharide-stimulated normal human lung fibroblast, epithelial cells, IPF fibroblast cells, and monocytes. Materials and methods: We detected CBRs in normal human lung fibroblasts (LL24) and IPF fibroblast cells (LL29), epithelial cells (A549) and monocytes (THP-1) by flow cytometry. We determined TGF-(31, IL-8, and TNF-alpha inflammatory cytokines in the LL24, LL29, A549, and THP-1 cell culture supernatants on days 1 and 5 by ELISA. We evaluated the cell viability in LL24, LL29, and A549 cells on days 1, 3, and 5 spectrophotometrically and detected collagen Type I (ColI) production in the LL24 and LL29 cell culture supernatants on days 1, 3, and 5 by ELISA. Results: LL24, LL29, A549, and THP-1 cells exhibited CB1 (CB1R) and CB2 (CB2R) receptors. CB1R and CB2R agonists WIN55,2122 and JWH015 inhibited fibroblastic and epithelial cell proliferation on day 5. TGF-(31 and TNF-alpha release increased, while IL-8 release decreased in LL24, LL29, A549, and THP-1 cells in response to the administration of WIN55,212-2 and JWH015 at a 10-2 mM concentration. CB1R and CB2R antagonists AM251 and AM630 did not block agonistic responses, suggesting a nonclassical CBRmediated pathway. CB2R agonist JWH015 decreased ColI expression in IPF lung fibroblasts LL29 on day 3. Conclusion: These results suggest that CB signaling regulates the progression of pulmonary inflammation and fibrosis via CBR activation. This may offer a potential pharmacological tool for developing antifibrosis therapies.
  • Thumbnail Image
    Conference Object
    A Cell Therapy Assisted Novel Microfluidic Device Promotes In Vitro Spermatogenesis in Neonatal Mice
    (Elsevier Science inc, 2022) Onen, Selin; Atik, Ali Can; Gizer, Merve; Kose, Sevil; Yaman, Onder; Kulah, Haluk; Korkusuz, Petek
  • Thumbnail Image
    Article
    Citation - WoS: 16
    Citation - Scopus: 19
    A Pumpless Monolayer Microfluidic Device Based on Mesenchymal Stem Cell-Conditioned Medium Promotes Neonatal Mouse in Vitro Spermatogenesis
    (Bmc, 2023) Onen, Selin; Atik, Ali Can; Gizer, Merve; Kose, Sevil; Yaman, Onder; Kulah, Haluk; Korkusuz, Petek
    BackgroundChildhood cancer treatment-induced gonadotoxicity causes permanent infertility/sub-infertility in nearly half of males. The current clinical and experimental approaches are limited to cryopreservation of prepubertal testicular strips and in vitro spermatogenesis which are inadequate to achieve the expanded spermatogonial stem/progenitor cells and spermatogenesis in vitro. Recently, we reported the supportive effect of bone marrow-derived mesenchymal cell co-culture which is inadequate after 14 days of culture in static conditions in prepubertal mouse testis due to lack of microvascular flow and diffusion. Therefore, we generated a novel, pumpless, single polydimethylsiloxane-layered testis-on-chip platform providing a continuous and stabilized microfluidic flow and real-time cellular paracrine contribution of allogeneic bone marrow-derived mesenchymal stem cells.MethodsWe aimed to evaluate the efficacy of this new setup in terms of self-renewal of stem/progenitor cells, spermatogenesis and structural and functional maturation of seminiferous tubules in vitro by measuring the number of undifferentiated and differentiating spermatogonia, spermatocytes, spermatids and tubular growth by histochemical, immunohistochemical, flow cytometric and chromatographic techniques.ResultsBone marrow-derived mesenchymal stem cell-based testis-on-chip platform supported the maintenance of SALL4(+) and PLZF(+) spermatogonial stem/progenitor cells, for 42 days. The new setup improved in vitro spermatogenesis in terms of c-Kit(+) differentiating spermatogonia, VASA(+) total germ cells, the meiotic cells including spermatocytes and spermatids and testicular maturation by increasing testosterone concentration and improved tubular growth for 42 days in comparison with hanging drop and non-mesenchymal stem cell control.ConclusionsFuture fertility preservation for male pediatric cancer survivors depends on the protection/expansion of spermatogonial stem/progenitor cell pool and induction of in vitro spermatogenesis. Our findings demonstrate that a novel bone marrow-derived mesenchymal stem cell-based microfluidic testis-on-chip device supporting the maintenance of stem cells and spermatogenesis in prepubertal mice in vitro. This new, cell therapy-based microfluidic platform may contribute to a safe, precision-based cell and tissue banking protocols for prepubertal fertility restoration in future.