Published customer image:
Mouse anti myelin proteolipid protein antibody, clone plpc1 used for the detection of proteolipid protein on formalin fixed, paraffin embedded brain tissue.
Image caption:
NL scheme and PLP staining. (A) Type-I NL with demyelination of the whole width of the cortex (#) and adjacent WM (*). (B) Type-II intracortical lesion evolving around a vessel. (C) Type-III subpial NL. Demyelination spreads from the pial surface until cortical layer 3. Scale bars represent 500 μm.

From:
Yao B, Hametner S, van Gelderen P, Merkle H, Chen C, et al. (2014)
7 Tesla Magnetic Resonance Imaging to Detect Cortical Pathology in Multiple Sclerosis.
PLoS ONE 9(10): e108863.

Published customer image:
Mouse anti myelin proteolipid protein antibody, clone plpc1 used for the detection of proteolipid protein on formalin fixed, paraffin embedded brain tissue.
Image caption:
NLs on MRI and tissue sections stained for PLP and iron. Examples Examples of NLs from tissue MS1 (A, B and C) identified on MRI magnitude (TE = 25.2 ms) and R2* images as well as color-coded PLP-staining and iron staining. Red arrows point towards NLs identified by MRI and confirmed to correspond to area of demyelination by the color-coded PLP staining. Blue arrows point towards NLs identified by the color-coded PLP staining and only retrospectively identified by MRI. Black arrows and black box point towards NLs identified by the color-coded PLP staining and not by MRI even upon a second retrospective image inspection. In the black box we include a large area of demyelination which goes entirely undetected by MRI. In the color-coded PLP staining of figure: green = complete WM demyelination, red = complete GM demyelination, yellow = areas of variably reduced myelin density.

From:
Yao B, Hametner S, van Gelderen P, Merkle H, Chen C, et al. (2014)
7 Tesla Magnetic Resonance Imaging to Detect Cortical Pathology in Multiple Sclerosis.
PLoS ONE 9(10): e108863.

Published customer image:
Mouse anti myelin proteolipid protein antibody, clone plpc1 used for the detection of proteolipid protein on formalin fixed, paraffin embedded brain tissue.
Image caption:
Iron loss in NLs. PLP myelin staining (B) and iron staining (C) on two consecutive slides of tissue MS2 disclose iron loss together with myelin loss in a NL (red arrows). Higher magnification (D, E, F, G) of PLP (D, F) and iron stainings (E, G). In NAGM (D, E), iron is present in oligodendrocytes (black arrow and inset in E) and myelin sheaths. In a NL (F, G), iron is removed from the demyelinated cortical parenchyma and present in perivascular macrophages and microglia (black arrow and inset in G).

From:
Yao B, Hametner S, van Gelderen P, Merkle H, Chen C, et al. (2014)
7 Tesla Magnetic Resonance Imaging to Detect Cortical Pathology in Multiple Sclerosis.PLoS ONE 9(10): e108863.

Published customer image:
Mouse anti myelin proteolipid protein antibody, clone plpc1 used for detection of myelin proteolipid protein in human and porcine brain lysates by western blotting
Image caption:
Validation of monomer and oligomer preference of αSN interacting proteins. Proteins pulled down by monomer αSN (M), oligomer αSN (O), and buffer control (B) from porcine (A-F) and human (G-I) brain extracts were analyzed by immunoblotting using antibodies against antigens selected among the monomer and oligomer binding proteins. Monomer binding antigens were myelin proteolipid protein (mPLP) and Abl interactor 1 (Abl1) and oligomer binding proteins were glial fibrillary acidic protein (GFAP), glutamate decarboxylase 2 (GAD2), and synapsin 1 (Syn1). VAMP-2 was tested because it has been reported to bind &apha;SN, although it was not detected in our proteomic analysis. One representative of three experiments is presented for porcine αSN binding proteins (A, C, E), and the quantification of the three experiments is presented in panels B, D, F. The quantification of bands was performed after subtracting the non-specific signal in the buffer control from the specific bands in monomer and oligomer samples. Bars represent mean ratio between monomer and oligomer ± S.D. of the three replicates. The values for binding to monomer and oligomer were compared by Student's t-test and the resulting p-values are listed above the bars. * Indicates that the band intensity from oligomer did not differ significantly from background making quantifications impracticable. In order to ensure that the interaction were not due to species differences between human and porcine proteins we conducted validations in human brain extracts. One representative of two experiments is presented for each validated protein. The validation for both porcine and human of mPLP, Abl1, Syn1 and VAMP-2 was conducted in the LP2 fraction enriched in synaptic vesicle and the validation to GFAP and GAD2 in the LS1 fraction of synaptosomal lysate.

From: Betzer C, Movius AJ, Shi M, Gai W-P, Zhang J, et al. (2015) Identification of Synaptosomal Proteins Binding to Monomeric and Oligomeric α-Synuclein.
PLoS ONE 10(2): e0116473.

Published customer image:Mouse anti myelin proteolipid protein antibody, clone plpc1 used for detection of proteolipid protein in formalin fixed, paraffin embedded multiple sclerosis brain tissue.
Image caption:
Microglia associated with preactive lesions express NADPH oxidase-2 subunits. Clusters of HLA-DR immunopositive microglia (B and C, HLA-DR) in NAWM (PLP, A) express various NADPH oxidase-2 subunits, including gp91phox (D), p22phox (E) and p47phox (F) in consecutive sections. Figure1C-F represents a magnification of the outlined square in Figure1B. Original magnifications A, B: 4×, C-F: 40×.

From: van Horssen J, Singh S, van der Pol S, Kipp M, Lim JL, Peferoen L, Gerritsen W, Kooi EJ, Witte ME, Geurts JJ, de Vries HE, Peferoen-Baert R, van den Elsen PJ, van der Valk P, Amor S.
Clusters of activated microglia in normal-appearing white matter show signs of innate immune activation.
J Neuroinflammation. 2012 Jul 2;9:156.

Published customer image:
Mouse anti myelin proteolipid protein antibody, clone plpc1 used for detection of proteolipid protein in formalin fixed, paraffin embedded multiple sclerosis brain tissue
Image caption:
Preactive lesions are composed of clusters of HLA-DR-positive microglia. In NAWM, i.e., in the absence of apparent myelin loss (A, E: proteolipid protein) preactive lesions are defined as circumscribed nodules of activated microglia expressing HLA-DR (B, C) and CD68 (D). Preactive lesions are predominantly observed in blocks containing active lesions (E: proteolipid protein; F, G: HLA-DR). Figure1G represents a magnification of the outlined square in (F). In some cases microglial nodules are surrounded by a halo devoid of microglia (H: HLA-DR). Original magnifications: A, B: 20×; C, D: 40×; E, F: 4×; G, H: 40×.

From: van Horssen J, Singh S, van der Pol S, Kipp M, Lim JL, Peferoen L, Gerritsen W, Kooi EJ, Witte ME, Geurts JJ, de Vries HE, Peferoen-Baert R, van den Elsen PJ, van der Valk P, Amor S.
Clusters of activated microglia in normal-appearing white matter show signs of innate immune activation.
J Neuroinflammation. 2012 Jul 2;9:156.

Published customer image:
Mouse anti myelin proteolipid protein antibody, clone plpc1 used for detection of myelin proteolipid protein in brain lysates by western blotting
Image caption:
Presence of &apha;SN binding proteins chosen for validation in synaptosomal fractions. 30μg of each of the fractions synaptosomal membranes LP1, synaptosomal lysate (LS1), synaptic vesicles (LP2) and synaptosomal cytosol (LS2) were immunoblotted, and analyzed for the presence of myelin Proteolipid protein (mPLP), Abl interactor 1 (Abl1), Glial fibrillary acidic protein (GFAP), Glutamic acid decarboxylase 2 (GAD2), Synapsin 1 (Syn1), and Vesicle associated membrane protein 2 (VAMP2).

From: Betzer C, Movius AJ, Shi M, Gai W-P, Zhang J, et al. (2015)
Identification of Synaptosomal Proteins Binding to Monomeric and Oligomeric α-Synuclein.
PLoS ONE 10(2): e0116473.

Published customer image:
Mouse anti Myelin proteolipid protein, clone plpc1 (MCA839G) used for the evaluation of PLP expression in human brain by immunohistochemistry on formalin fixed, paraffin embedded biopsy sections.
Image caption:
LRP1 expression is increased in MS lesions. a Immunohistochemistry on consecutive sections from an early active (EA) MS lesion (upper row) shows: (1) myelin (PLP) laden macrophages consistent with ongoing demyelinating activity, (2) abundant macrophage infiltration (CD68), (3) hypertrophic reactive astrocytes indicating gliosis (GFAP), and (4) LRP1 immunoreactivity present on both astrocytes (arrowhead) and macrophages (arrow and inset). In contrast, the periplaque gray matter (PPGM, lower row) shows: (1) normal appearing myelin (PLP), (2) limited microglial reactivity (CD68), (3) astrocytes with regular size and morphology (GFAP), and (4) limited LRP1 immunoreactivity. (Scale bars?=?20 μm). b Luxol Fast Blue histology (LFB) and immunofluorescence for CD68 and LRP1 shows that myeloid cells express LRP1 within the lesion (Scale bar?=?100 μm)

From: Chuang TY, Guo Y, Seki SM, Rosen AM, Johanson DM, Mandell JW, Lucchinetti CF, Gaultier A.
LRP1 expression in microglia is protective during CNS autoimmunity.
Acta Neuropathol Commun. 2016 Jul 11;4(1):68.

Published customer image:
Mouse anti myelin proteolipid protein antibody, clone plpc1 (MCA839G) used for the evaluation of PLP expression in human brain by immuohistochemistry on formalin fixed, paraffin embedded tissue sections.
Image caption:
Basic Pathology of HAE: a: Topographical distribution of demyelinated lesions in the brain shows the prominent periventricular demyelination with peri-venous extensions (Dawson Fingers) and demyelinated plaques in the cortex and the deep grey matter nuclei; green: white matter lesions, red: cortical and hippocampal lesions, blue: lesions in thalamus and basal ganglia; the blue dots in the meninges show the location of prominent meningeal inflammatory infiltrates; b: Sections stained with luxol fast blue depicts the demyelinated lesions in the white matter; c: Immunocytochemistry for CD68 shows the accumulation of macrophages at the edge of active white matter lesions; d: Double staining for proteolipid (PLP) protein (red) and mRNA (black) reveals loss of oligodendrocytes within the lesion and the presence of numerous macrophages with PLP degradation products at the lesion edge; e: In sections stained for phosphorylated neurofilament only a mild to moderate reduction of axonal density is seen in the lesions; the insert shows a neuron in the substantia nigra with an α-synuclein reactive Lewy body. f: The section stained for iron shows prominent iron accumulation in the deep grey matter nuclei and at the cortico/subcortical border; some increased iron reactivity is seen within the periventricular demyelinated lesions: g: Subpial cortical lesion in the insular cortex (Fig. 1a) with selective loss of myelin in the cortex; h, i: The subpial lesions shows an actively demyelinating edge with high density of activated microglia (Iba-1, Fig. 1h), expressing the phagocytosis associated marker CD68 (Fig. 1i). j, k: In the meninges, covering the active lesion, inflammatory infiltrates are seen, composed or perivascular T-cells (CD3, Fig. 1j) and B-cells (CD20, Fig. 1k); l: The active lesion edge of the cortical lesions contains numerous macrophages with PLP reactive myelin degradation products; m: Activated microglia and macrophages at the lesions edge express NADPH oxidase.

From: Höftberger R, Leisser M, Bauer J, Lassmann H.
Autoimmune encephalitis in humans: how closely does it reflect multiple sclerosis?
Acta Neuropathol Commun. 2015 Dec 4;3:80.