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  Table of Contents    
ORIGINAL ARTICLE  
Year : 2012  |  Volume : 55  |  Issue : 1  |  Page : 56-60
Immunohistochemical study of osteopontin, Ki-67, and CD34 of psoriasis in Mansoura, Egypt


1 Department of Pathology, Mansoura Faculty of Medicine, Mansoura, Egypt
2 Department of Dermatology, Mansoura Faculty of Medicine, Mansoura, Egypt

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Date of Web Publication11-Apr-2012
 

   Abstract 

Background and Objective: Psoriasis is a chronic inflammatory skin disease characterized by hyper-proliferation, abnormal differentiation, and inflammatory infiltration in epidermis and dermis. We planned this study to analyze probable associations between Osteopontin (OPN), Ki-67, CD34, and histopathological features in psoriasis. Materials and Methods: We studied OPN expression and its correlation with Ki-67 and CD34 expression in lesional, non-lesional skin, and normal skin. Immunoreactivity for OPN and Ki-67 was based on the level of epidermal staining. CD34 expression was scored as mild, moderate, and strong, according to the number of stained dermal capillaries. Results: Our results showed statistically significant differences in the expression of OPN, Ki-67, and CD34 between lesional and non-lesional skin as well as between non-lesional skin and control group (P≤0.001). In addition, there was a significant difference in the expression of OPN, Ki-67, and CD34 between control and lesional group (P=0.02, P=0.02, and P=0.04, respectively). Conclusions: OPN expression seems to be related to Ki-67 (proliferation index) and CD34 expression (angiogenesis marker) confirming its role in the pathogenesis of psoriasis. Then "anti- OPN and anti-angiogenesis" may eventually become a useful therapeutic approach in psoriasis.

Keywords: CD34, Ki-67, osteopontin, psoriasis

How to cite this article:
Amin MM, Azim ZA. Immunohistochemical study of osteopontin, Ki-67, and CD34 of psoriasis in Mansoura, Egypt. Indian J Pathol Microbiol 2012;55:56-60

How to cite this URL:
Amin MM, Azim ZA. Immunohistochemical study of osteopontin, Ki-67, and CD34 of psoriasis in Mansoura, Egypt. Indian J Pathol Microbiol [serial online] 2012 [cited 2019 Dec 12];55:56-60. Available from: http://www.ijpmonline.org/text.asp?2012/55/1/56/94857



   Introduction Top


Osteopontin (OPN) is a phosphorylated acidic glycoprotein originally found in bone and known to be involved in the formation and calcification of bone. It is expressed in activated macrophages, T cells, osteoclasts, hepatocytes, endothelial and epithelial cells. OPN has important roles in normal physiological as well as pathological processes. It was originally classified as a T-helper type 1 cytokine that was involved in mineralization of bone and kidney, cell survival, inflammation, and tumor biology. OPN induces the expression of other pro-inflammatory cytokines and chemokines in peripheral blood mononuclear cells. Moreover, it has a role in cell migration and stimulates expression of metalloproteases to induce matrix degradation and facilitates cell motility. It was suggested that OPN plays a role in many diseases characterized by chronic inflammation, including psoriasis, Crohn's disease, several types of cancers, autoimmune diseases, obesity, atherosclerosis, and cardiac fibrosis. [1]

Expression of OPN in a variety of tissues indicates a multiplicity of functions. A definitive role for OPN in any tissue studied has provided some new addition to the role of this protein in variable biological events, including developmental processes, wound healing, immunological responses, tumorigenesis, bone resorption, and calcification. [2]

OPN is secreted in autoimmune diseases such as lupus erythematosus, and influences inflammation of immediate and delayed type allergies and granuloma formation through cytokine functions. [3],[4] It supports immune responses against mycobacteria and viruses such as herpes simplex virus. OPN is also implicated in skin tumors and its over-expression influences invasion and metastasis of melanoma and squamous cell carcinoma. [2] OPN is predominantly known as a secreted protein; however, an intracellular form, iOPN, had gained much attention in immune cell signaling and cell migration. [5]

Psoriasis is an immune mediated inflammatory disease with a genetic basis in which Th1 and Th17-mediated inflammation have been proposed to be pathogenically essential. [6] Because of the impact of OPN on Th1 / Th17 immune responses in autoimmunity, Chen et al. [7] hypothesized that OPN is of pathogenic importance in psoriasis and demonstrated that increased OPN levels were significantly associated with psoriasis, hypertension, and diabetes mellitus.

This study was conducted to verify the role of OPN in the development of psoriasis and also to study the role of Ki-67 and CD34 in the pathogenesis of psoriasis.


   Materials and Methods Top


Patients

This study was performed on 14 patients (7 male and 7 female) with psoriasis vulgaris, attending Dermatology Clinic of Our University Hospital with age range from 7-50 years. [Table 1] This work had been approved by Ethics Committee of our University. Psoriasis was diagnosed by clinical features and histology. Patients did not receive topical or systemic therapy of psoriasis for at least two months prior to the study. From every patient, elliptical biopsy was taken from skin unexposed to sunlight involving lesional and non-lesional skin. The biopsy was cut into two portions; one involving psoriatic lesion and the other involving the peri-lesional normally appearing skin. Ten specimens from foreskin (during circumcision) of normal persons were used as controls. Informed consent was taken from all participants.
Table 1: Clinical data of psoriatic patients

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Immunohistochemical and Histochemical Analysis

Staining procedure

All specimens were fixed in formalin 10% and 4-6 μm sections were cut on glass slides for routine H and E staining. Sections were deparaffinized and rehydrated through graded alcohols to water, Avidin-Biotin-Peroxidase method and 3,3-diaminobenzidine (DAB) chromogen were applied for immunohistochemical analysis. Endogenous peroxidase activity was blocked with 0.6% H 2 O 2 . After blocking, sections were incubated at room temperature for 60 min with antibodies to human Osteopontin (Dako, Rabbit PAb RB- 9097-R1 53, Fremont, CA, USA), Ki-67 (Dako, Monoclonal Mouse Anti-Human Ki-67 Antigen, Code M7240 and Clone MIB-1, UK), and CD34 (Dako, Mouse Anti-Human CD34 Antigen, code K4004 and Clone: QBEnd-10, USA). Specimen from cancer breast was used as positive controls for OPN. Epidermal basal cells provided as positive control for Ki-67 and OPN. Negative controls for all studies were obtained by omission of the primary antibodies. OPN showed cytoplasmic staining and CD34 showed cytoplasmic and membranous staining, while Ki-67 showed nuclear staining. All samples that were stained with Hematoxylin and Eosin and the immunohistochemical markers were examined by Olympus light microscope.

Evaluation

The degree of immunoreactivity for OPN and Ki-67 were evaluated according to the level of epidermal staining; three groups were distinguished; [8] basal only, lower half of the epidermis, and whole epidermis [Table 2]; but evaluation of staining in CD34 (microvessel density; MVD) was performed by capillary counting in the 3 most highly vascularized areas initially selected (i.e. the so-called hot spots) under 40x field. Then a 400x field was used to count microvessels in each of these areas. Single or clusters of endothelial cells, with or without lumen, were considered to be individual vessels [9] and scored as follows: Mild (4-10 capillary), moderate (11-20 capillary), and sever (21-28 capillary).
Table 2: Results of immunohistochemistry in osteopontin and ki67

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Statistical Analysis

The distribution of parameters was characterized by standard descriptive methods. The nonparametric Mann-Whitney Z test were used to analyze nonparametric variables and to compare between different groups (lesional, non lesional, and control). Spearman rank Correlation Coefficient r with P value was used to correlate between OPN, Ki-67, and CD34 in lesional and non lesional skin. Two-tailed P values of ≤0.05 were considered statistically significant.


   Results Top


The clinical data of psoriatic patients were shown in [Table 1]. Typical histological features of psoriasis vulgaris include regular acanthosis, papillomatosis, hypogranulosis, hyperkeratosis, and parakeratosis along with characteristic micro-abscess formation with vascular changes. The results of immunohistochemical study were summarized in [Table 2] and [Table 3].
Table 3: Results of immunohistochemistry in CD34

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Expression of osteopontin

OPN in normal skin was limited to the basal cell layer, hair follicles, sebaceous glands, and sweat glands. OPN positive reactivity was observed in all samples of lesional psoriatic skin and distributed throughout the epidermis at various levels. It was also expressed in the inflammatory cells and microvasculature endothelial cells of the dermis in all cases [Figure 1]a. In non lesional skin, OPN expression was detected in the epidermis of 71.4% of cases and at lower level [Figure 1]b. Positive staining of less intensity was observed in lymphocytes and microvasculature endothelial cells of the dermis in 5 cases only (35.7%). There were statistically significant differences in OPN expression between lesional and non-lesional skin as well as between non-lesional and control group (Z=3.8, P≤0.001and Z=4.1, P≤0.001, respectively). There was also significant difference in OPN expression between lesional skin and control group (Z=2.3, P=0.02).
Figure 1: Immunohistochemical staining of Osteopontin in lesional skin (a) and non lesional skin (b) of psoriasis, a: (IHC, ×200) and b: (IHC, ×400)

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Expression of Ki-67

Ki-67 expression was seen only in the nuclei of epidermal cells and no stained cells were detected in the dermis. In control group, it was present in the basal cell layer only. In psoriatic lesions, positive reactivity was observed in all samples with various levels [Figure 2]a. In non-lesional skin, Ki-67 expression was detected in all cases but at lower level [Figure 2]b. The differences between lesional and non-lesional skin as well as between non-lesional skin and control group were statistically significant (Z=3.7, P≤0.001 and Z=4.1, P≤0.001, respectively). Also, there was significant difference between lesional skin and control group (Z=2.3, P=0.02) [Table 4]. Ki-67 was also detected in epidermal inflammatory cell population of psoriatic lesions, but most of the dermal cells were Ki-67 negative.
Figure 2: Immunohistochemical staining of Ki- 67 in lesional skin (a) and non lesional skin (b) of psoriasis: (IHC, ×200)

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Table 4: Comparison between osteopontin, Ki67 and CD34 expression Z of Mann-Whitney Z test

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CD34 Expression

CD34 was observed in psoriatic lesions in all samples with various intensities [Figure 3]a. In non-lesional skin, CD34 expression was also present in all cases but with lesser intensities [Figure 3]b. In the control normal skin, CD34 expression was weak in all cases. CD34 expression in lesional skin was significantly higher than in non-lesional skin (Z=2.6, P≤0.01). Also, there was statistically significant differences between non-lesional and control group (Z=3.6, P≤0.001) as well as between control and lesional group (Z=2.1, P=0.04) [Table 4].
Figure 3: Immunohistochemical staining of CD34 in lesional skin (a) and non lesional skin (b) of psoriasis: (IHC, ×400)

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In lesional skin, there was non-significant correlation between OPN and Ki-67 expression (r=0.3, P<0.05), but there was statistically significant correlation between OPN and CD34 expression (r=0.7, P<0.01) as well as between CD34 and Ki-67 (r=0.5, P<0.05). In non-lesional skin, there was no statistically significant correlation between OPN and Ki-67 expression as well as between OPN and CD34 (r=0.4, P<0.05 in both). Also, no statistically significant correlation was found between CD34 and Ki-67 expression (r=-0.04, P<0.05) [Table 5].
Table 5: Correlation coefficient (r with P value) between osteopontin, Ki 67 levels and CD34 in lesional and nonlesional skin of psoriatic patients

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   Discussion Top


Psoriasis is characterized by epidermal hyperproliferation with abnormal differentiation and inflammatory infiltration of epidermis and dermis. The growth pattern of psoriatic skin tissue differs from normal by the great decrease in transit time of cells from the basal cell layer to the uppermost of the squamous cell layer. [10],[11] In addition to the possible role of OPN in differentiation, it is also important for enhancing cell survival, especially during the time of external or internal stress, because numerous in vitro and in vivo studies support its role in preventing stress-induced cell apoptosis. [12]

In the present study, OPN was significantly expressed throughout the epidermis of psoriatic lesion (P≤0.001), which was minimally expressed only in the basal cell layer of normal skin. These results were in agreement with Wrone-Smith et al. [13] The authors stated that, in normal human skin, kertinocytes in the superficial layer of the epidermis undergo apoptosis and there was proliferation of cells in the basal layer. As opposed to normal skin, kertinocytes derived from psoriatic plaques were shown to be resistant to apoptosis. Also, inappropriate regulation of apoptosis was proposed as a possible explanation for epidermal thickening in hyperproliferative inflammatory skin disorders including psoriasis. [14]

In present study, OPN was also positive in 71.4% only of non lesional skin and at lower level than lesional skin. These results, possibly indicating that in some psoriatic patients, non lesional skin might be predisposed to develop the disease.

In our study, the expression of OPN in dermal inflammatory cells of psoriatic lesion was detected and this was explained by Wang and Denhardt. [15] The authors stated that the chemotactic soluble OPN attracts other immune cells to the inflammatory sites such as dentritic cell (DC), neutrophils, natural killer (NK) cells, NK-T cells, and macrophages, which are all known to migrate towards OPN. Also, in agreement with our study, Renkl et al. [16] demonstrated that OPN encountered by dendritic cells in the dermal matrix activates and polarizes langerhans cell (LC) and myeloid DC towards a Th1 phenotype, thereby stabilizing the inflammatory Th1 response. OPN was also synthesized by various immune cells such as macrophages, dendritic cells, natural killer cells, T cells, and B cells. [17] These observations support our results that OPN is expressed in the dermal inflammatory cells of lesional and non-lesional skin of psoriatic patient.

Ki-67 was a widely used marker to detect S, G2, and M phases of the cell cycle. [10] Over- expression of Ki-67 in the epidermis of psoriatic lesions in the present study was significantly higher than in non-lesional skin (P≤0.001) which may be regarded as a major finding that points out epidermal hyperproliferation and this was coincides with that observed by Jun-min, et al. [18] These authors observed that the over-expression of Ki-67 and PCNA in psoriatic lesions suggests that there is an abnormality of cell cycle regulation of psoriatic kertinocytes. The abnormality might be related to the hyper-proliferation and abnormal differentiation of psoriatic kertinocytes, implying that it may be involved in the pathogenesis of psoriasis. The findings of this study were also in accordance with the observations that show Ki-67 staining as a notable indicator for psoriatic epidermis. [19],[20]

Ki-67 is an important marker of active cycling cells in psoriasis. A large body of evidence indicates that the cell cycle time in psoriasis is normal and only increased recruitment of epidermal cells is responsible for the development of psoriatic lesions. [21] In this study, Ki-67 positive inflammatory cells in the epidermis and Ki-67 negative dermal cells are in agreement with Nickoloff and Griffiths. [22] The authors suggested that dermal T-cells are in a resting or non-cycling (Go) state and the entry of the T cells into the epidermis is, therefore, apparently associated with an important activation event, which involves interaction with the kertinocytes.

In the present study, CD34 expression in the endothelial cells of lesional skin was significantly higher than in non lesional skin (P≤0.01) and OPN was also expressed in endothelial cell of the psoriatic patients and these finding was explained by Gürsoy et al., [23] The authors stated that OPN had been involved in the onset of angiogenesis through a mechanism mediated by interleukin-1 (IL-1) by acting directly on endothelial cells and/or indirectly via mononuclear phagocyte engagement. The local release of angiogenic growth factors is responsible for the uncontrolled endothelial cell proliferation that takes place during tumor neo-vascularization and in angiogenesis dependent disease such as diabetic retinopathy, psoriasis, rheumatoid arthritis. Also, Giachelli and Steitz, [24] noticed that OPN is expressed in proliferating and migratory vascular cells associated with neo-intima formation and in inflammatory cells.

Our results suggest that OPN is a pleiotropic cytokine that functions both systemically and locally in tissue. In agreement with our study, Konno et al. [25] observed that OPN was able to exert its effects through different functional domains, and the secreted and intracellular forms of OPN may have distinct functions. OPN plays multiple roles in the regulation of allergic responses and asthma, including regulation of IgE response, inflammatory cell migration, and the development of airway fibrosis and angiogenesis.


   Conclusion Top


OPN expression in psoriasis seems to be related to Ki-67 and CD34 expression supporting its role in the pathogenesis of psoriasis. Then "anti-OPN and anti-angiogenesis" may eventually become a useful therapeutic approach in psoriasis. Future research to study all aspects of OPN function is needed to establish its role in the regulation of immune responses and various disease processes.


   Acknowledgments Top


We thank the participants from outpatient clinic of dermatology department for their cooperation. We also thank Hatem Abdel Barry for his technical assistance.

 
   References Top

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2.Sodek J, Ganss B, McKee MD. Osteopontin. Crit Rev Oral Biol Med 2000;11:279-303.  Back to cited text no. 2
    
3.Ashkar S, Weber GF, Panoutsakopoulou V, Sanchirico ME, Jansson M, Zawaideh S, et al. Eta-1 (Osteopontin): An early component of type-1 (cell-mediated) immunity. Science 2000;287:860-4.   Back to cited text no. 3
    
4. O'Regan AW, Hayden JM, Berman JS. Osteopontin augments CD3-mediated interferon-γ and CD40 ligand expression by T cells, which results in IL-12 production from peripheral blood mononuclear cells. J Leukoc Biol 2000;68:495-502.  Back to cited text no. 4
    
5.Shinohara ML, Lu L, Bu J, Werneck MB, Kobayashi KS, Glimcher LH, et al. Osteopontin expression is essential for interferon-alpha production by plasmacytoid dendritic cells. Nat Immunol 2006;7:498-506.  Back to cited text no. 5
    
6.Zaba LC, Fuentes-Duculan J, Eungdamrong NJ, Abello MV, Novitskaya I, Pierson KC, et al. Psoriasis is characterized by accumulation of immunostimulatory and Th1 / Th17 cell-polarizing myeloid dendritic cells. J Invest Dermatol 2009;129:79-88.  Back to cited text no. 6
    
7.Chen YJ, Shen JL, Wu CY, Chang YT, Chen CM, Lee FY, et al. Elevated plasma Osteopontin level is associated with occurrence of psoriasis and is an unfavorable cardiovascular risk factor in patients with psoriasis. J Am Acad Dermatol 2009;60:225-30.  Back to cited text no. 7
    
8.Doger FK, Dikicioglu E, Ergin F, Unal E, Sendur N, Uslu M, et al. Nature of cell kinetics in psoriatic epidermis. J Cutan Pathol 2007;34:257-63.  Back to cited text no. 8
    
9.Ding S, Li C, Lin S, Yang Y, Liu D, Han Y, et al. Comparative evaluation of microvessel density determined by CD34 or CD105 in benign and malignant gastric lesions. Hum Pathol 2006;37:861-6.  Back to cited text no. 9
    
10.Kawashima K, Doi H, Ito Y, Shibata M, Yoshinaka R, Otsuki Y, et al. Evaluation of cell death and proliferation in psoriatic epidermis. J Dermatol Sci 2004;35:207-14.  Back to cited text no. 10
    
11.Mobini N, Toussaint S, Kamino H. Psoriasis. In: Lever's Histopathology of the Skin (Elder DE, Elenitsas R, Johnson BL Jr, Murphy GF, editors. 10 th ed. Philadelphia, PA; Lippincott Williams and Wilkins; 2009. p. 174-81.  Back to cited text no. 11
    
12.Hsieh YH, Juliana MM, Hicks PH, Feng G, Elmets C, Liaw L, et al. Papilloma development is delayed in Osteopontin-null mice: Implicating an antiapoptosis role for Osteopontin. Cancer Res 2006;66:7119-27.  Back to cited text no. 12
    
13.Wrone-Smith T, Mitra RS, Thompson CB, Jasty R, Castle VP, Nickoloff BJ, et al. Keratinocytes derived from psoriatic plaques are resistant to apoptosis compared with normal skin. Am J Pathol 1997;151:1321-9.  Back to cited text no. 13
    
14.Koçak M, Bozdogan O, Erkek E, Atasoy P, Birol A. Examination of Bcl-2, Bcl-X and bax protein expression in psoriasis. Int J Dermatol 2003;42:789-93.  Back to cited text no. 14
    
15.Wang KX, Denhardt DT. Osteopontin: Role in immune regulation and stress responses. Cytokine Growth Factor Rev 2008;19:333-45.  Back to cited text no. 15
    
16.Renkl AC, Wussler J, Ahrens T, Thoma K, Kon S, Uede T, et al. Osteopontin functionally activates dendritic cells and induces their differentiation towards a Th-1 polarizing phenotype. Blood 2005;106:946-55.  Back to cited text no. 16
    
17.Denhardt DT, Noda M, O'Regan AW, Pavlin D, Berman JS. Osteopontin as a means to cope with environmental insults: Regulation of inflammation, tissue remodeling, and cell survival. J Clin Invest 2001;107:1055-61.  Back to cited text no. 17
    
18.Jun-min Z, Geng-shi H, Chun-hong Z. Expression of P57 (kip2), PCNA and Ki67 in psoriatic lesion. J Chin Trop Med 2009;9:453.  Back to cited text no. 18
    
19.Gudjonsson JE, Johnston A, Sýgmundsdottýr H, Valdýmarsson H. Immunopathogenic mechanisms in psoriasis. Clin Exp Immunol 2004;135:257-63.  Back to cited text no. 19
    
20.Walsh DS, Borke JL, Balagon MV. Psoriasis is characterized by altered epidermal expression of caspase 14, a novel regulator of keratinocyte terminal differentiation and barrier formation. J Dermatol Sci 2005;37:61-3.  Back to cited text no. 20
    
21.Kerkhof P. Texbook of psoriasis. Oxford: Blackwell Publishing Ltd.; 2003. p. 83-109.  Back to cited text no. 21
    
22.Nickoloff BJ, Griffiths CE. Lymphocyte trafficking in Psoriasis: A New Perspective Emphasizing the Dermal Dendrocyte with Active Dermal Recruitment Mediated via Endothelial Cells Followed by Intra-Epidermal T-Cell Activation. J Investig Dermatol 1990;95:35S-7S.  Back to cited text no. 22
    
23.Gürsoy G, Acar Y, Alagöz S. Osteopontin: A multifunctional molecule. J Med Med Sci 2010;1:55-60.  Back to cited text no. 23
    
24.Giachelli CM, Steitz S. Osteopontin: A versatile regulator of inflamation and biomineralization. Matrix Biol 2000;19:615-22.  Back to cited text no. 24
    
25.Konno S, Kurokawa M, Uede T, Nishimura M, Huang SK. Role of Osteopontin, a multifunctional protein, in allergy and asthma. Clin Exp Allergy 2011;7:93-109.  Back to cited text no. 25
    

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Correspondence Address:
Maha Mohamed Amin
Mansoura Faculty of Medicine
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0377-4929.94857

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    Figures

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    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]

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